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lncRNA MIR17HG调节miR-214-3p/RNF38信号轴对肝癌细胞恶性生物学行为的影响
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作者 孙伟涛 石彦科 +2 位作者 封俊连 陈志飞 张存岭 《现代消化及介入诊疗》 2024年第5期565-571,共7页
目的探究长链非编码RNA(lncRNA)人类微小RNA17簇宿主基因(MIR17HG)调节微小RNA(miR)-214-3p/环指蛋白38(RNF38)信号轴对肝癌细胞恶性生物学行为的影响。方法收集2022年5月至2023年10月于本院行手术切除的46例肝癌患者的癌组织及癌旁组织... 目的探究长链非编码RNA(lncRNA)人类微小RNA17簇宿主基因(MIR17HG)调节微小RNA(miR)-214-3p/环指蛋白38(RNF38)信号轴对肝癌细胞恶性生物学行为的影响。方法收集2022年5月至2023年10月于本院行手术切除的46例肝癌患者的癌组织及癌旁组织,检测lncRNA MIR17HG、miR-214-3p和RNF38的表达。体外培养HepG2、Bel-7402、SMMC-7721、HL-7702细胞,并比较lncRNA MIR17HG、miR-214-3p和RNF38的表达,选择Bel-7402细胞继续研究,随机分为sh-NC组、sh-MIR17HG组、anti-NC组、anti-miR-214-3p组和Bel-7402组。探究各组Bel-7402细胞增殖、凋亡、侵袭和迁移情况,蛋白质印迹法分析RNF38、半胱天冬酶-3(caspase-3)、B细胞淋巴瘤-2(Bcl-2)、基质金属蛋白酶-2(MMP2)、基质金属蛋白酶-9(MMP9)蛋白表达,双荧光素酶验证lncRNA MIR17HG与miR-214-3p以及miR-214-3p与RNF38的关系。结果肝癌组织中lncRNA MIR17HG、RNF38的mRNA表达较高,miR-214-3p的mRNA表达较低,RNF38的蛋白阳性表达率较高(P<0.05)。细胞SMMC-7721、HepG2、Bel-7402中lncRNA MIR17HG mRNA、RNF38 mRNA和RNF38蛋白表达高于HL-7702细胞,miR-214-3p mRNA表达低于HL-7702细胞(P<0.05)。与Bel-7402组、sh-NC组比较,sh-MIR17HG组OD 450nm值、克隆细胞数、侵袭细胞数、迁移细胞数和RNF38、MMP2、Bcl-2、MMP9表达减少,凋亡率和caspase-3表达增加(P<0.05);与sh-MIR17HG组、anti-NC组比较,anti-miR-214-3p组OD 450nm值、克隆细胞数、侵袭细胞数、迁移细胞数和RNF38、MMP2、Bcl-2、MMP9表达增加,凋亡率和caspase-3表达减少(P<0.05)。lncRNA MIR17HG与miR-214-3p以及miR-214-3p与RNF38分别存在靶向关系。miR-214-3p+WT-MIR17HG组荧光素酶活性低于miR-NC+WT-MIR17HG组(P<0.05),miR-214-3p+WT-RNF38组荧光素酶活性低于miR-NC+WT-RNF38组(P<0.05)。结论lncRNA MIR17HG可能通过调控miR-214-3p/RNF38轴促进肝癌细胞的恶性生物学行为。 展开更多
关键词 长链非编码RNA 人类微小RNA17簇宿主基因 miR-214-3p/环指蛋白38 肝癌 恶性生物学
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葡萄扇叶病毒杭州分离物(GFLV-H)P_(38)蛋白基因克隆及序列分析 被引量:1
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作者 李红叶 陈力耕 周雪平 《浙江大学学报(农业与生命科学版)》 CAS CSCD 北大核心 2003年第1期34-38,共5页
为了证实GFLV-HP38蛋白的性质及其在寄主扩散中的作用,根据葡萄扇叶病毒(Grapevinefanleafvirus,GFLV)法国分离物F13RNA2序列合成特异性引物,利用RT-PCR从GFLV-H基因组中扩增出P38蛋白基因的cDNA片段,并克隆到pGEM-T-easyvector上。序... 为了证实GFLV-HP38蛋白的性质及其在寄主扩散中的作用,根据葡萄扇叶病毒(Grapevinefanleafvirus,GFLV)法国分离物F13RNA2序列合成特异性引物,利用RT-PCR从GFLV-H基因组中扩增出P38蛋白基因的cDNA片段,并克隆到pGEM-T-easyvector上。序列分析表明该基因包含1044个核苷酸,编码347个氨基酸。序列比较发现GFLV-HP38蛋白基因与GFLV-F13对应基因核苷酸和氨基酸的同源性分别为90%和96%;与线虫传多面体病毒属中的南芥菜花叶病毒(Arabismosaicvirus,ArMV)和番茄环斑病毒(Tomatoringspotvirus,TomRSV)对应基因氨基酸同源性分别为85%和38.6%,与烟草黑环病毒(Tabaccoblackringvirus,TBLV)、葡萄铬色花叶病毒(Grapevinechromemosaicvirus,GCMV)和树莓环斑病毒(Raspberryringspotvirus,RRSV)的同源性均低于30%。 展开更多
关键词 葡萄扇叶病毒 杭州分离物 p38蛋白 基因克隆 同源性 序列分析
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Involvement of ERK1/2 and p38 MAPK in up-regulation of 14-3-3 protein induced by hydrogen peroxide preconditioning in PC12 cells
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作者 苏庆杰 陈小武 +1 位作者 陈志斌 孙圣刚 《Neuroscience Bulletin》 SCIE CAS CSCD 2008年第4期244-250,共7页
Objective To investigate the protective effects of hydrogen peroxide preconditioning (HPP) on the pheochromocytoma (PC12) cells treated with 1-methyl-4-phenylpyridinium (MPP^+) and to explore the potential mech... Objective To investigate the protective effects of hydrogen peroxide preconditioning (HPP) on the pheochromocytoma (PC12) cells treated with 1-methyl-4-phenylpyridinium (MPP^+) and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 4′,6′-diamidino-2-phenylindole (DAPI) staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase (MAPK) were determined by Western blot. Enzyme-linked immunosorbent assay (ELISA) was used to measure the activity of extracellular signal-regulated protein kinase 1/2 (ERK1/2). Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^+ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^+- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP+ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways. 展开更多
关键词 hydrogen peroxide preconditioning 14-3-3 protein ERK1/2 p38 mitogen-activated protein kinase pC12 cell
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IL-12、LPS对肾小管上皮细胞中lck/P_(38)信号传递的影响
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作者 李清刚 李幼姬 +1 位作者 李志坚 黄凌虹 《中山医科大学学报》 CSCD 2000年第3期190-192,共3页
【目的】探讨IL 12、LPS对肾小管上皮细胞中lck基因表达及活性改变的影响 ,明确lck/P3 8信号传递途径在炎症过程的作用。【方法】用原位杂交、放射自显影分别检测lck基因表达及lck活性 ,用免疫印迹法对肾小管上皮细胞在IL 12、LPS刺激下... 【目的】探讨IL 12、LPS对肾小管上皮细胞中lck基因表达及活性改变的影响 ,明确lck/P3 8信号传递途径在炎症过程的作用。【方法】用原位杂交、放射自显影分别检测lck基因表达及lck活性 ,用免疫印迹法对肾小管上皮细胞在IL 12、LPS刺激下其P3 8磷酸化进行测定。【结果】肾小管上皮细胞经IL 12 ,LPS刺激后lckmRNA表达水平增高 ,lck活性在刺激后 5min时最强 ,加入lck抑制剂PP1,IL 12刺激lck活性明显减弱。IL 12及LPS可以促进肾小管上皮细胞中P3 8活化、磷酸化 ,在 15min时最强 ,加入lck抑制剂后则抑制IL 12刺激时的P3 8磷酸化 ,而LPS刺激组不明显。【结论】IL 12 ,LPS可通过促进肾小管上皮细胞中lck/P3 8活化 ,参与炎症过程。 展开更多
关键词 肾小管 上皮细胞 白细胞介素12 脂多糖 LpS LCK
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Inhibition of p38 mitogen-activated protein kinase may decrease intestinal epithelial cell apoptosis and improve intestinal epithelial barrier function after ischemia- reperf usion injury 被引量:8
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作者 Shu-YunZheng Xiao-BingFu +3 位作者 Jian-GuoXu Jing-YuZhao Tong-ZhuSun WeiChen 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第5期656-660,共5页
AIM: To investigate the role of p38 mitogen-activated protein kinase in rat small intestine after ischemia-reperfusion (I/R)insult and the relationship between activation of p38 MAPK and apoptotic cell death of intest... AIM: To investigate the role of p38 mitogen-activated protein kinase in rat small intestine after ischemia-reperfusion (I/R)insult and the relationship between activation of p38 MAPK and apoptotic cell death of intestine.METHODS: Ninety Wistar rats were divided randomly into three groups, namely sham-operated group (C), I/R vehicle group (R) and SB203580 pre-treated group(S).In groups R and S, the superior mesenteric artery(SMA)was separated and occluded for 45 min, then released for reperfusion for0.25, 0.5, 1, 2, 6, 12 and 24 h. In group C, SMA was separated without occlusion. Plasma D-lactate levels were examined and histological changes were observed under a light microscope. The activity of p38 MAPK was determined by Western immunoblotting and apoptotic cells were detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUDP-biotin nick end labeling (TUNEL).RESULTS: Intestinal ischemia followed by reperfusion activated p38 MAPK, and the maximal level of activation (7.3-fold vs sham-operated group) was reached 30 min after I/R. Treatment with SB 203580, a p38 MAPK inhibitor,reduced intestinal apoptosis (26.72±3.39% vs62.50±3.08%in I/R vehicle, P<0.01) and decreased plasma D-lactate level (0.78±0.15 mmol/L in I/R vehicle vs0.42±0.17 mmol/L in SB-treated group) and improved post-ischemic intestinal histological damage.CONCLUSION: p38 MAPK plays a crucial role in the signal transduction pathway mediating post-ischemic intestinal apoptosis, and inhibition of p38 MAPK may attenuate ischemia-reperfusion injury. 展开更多
关键词 INTESTINES Ischemia-reperfusion injury p38 mitogen-activated protein kinase ApOpTOSIS
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Electroacupuncture reduces apoptotic index and inhibits p38 mitogen-activated protein kinase signaling pathway in the hippocampus of rats with cerebral ischemia/reperfusion injury 被引量:18
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作者 Xiao Lan Xin Zhang +3 位作者 Guo-ping Zhou Chun-xiao Wu Chun Li Xiu-hong Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第3期409-416,共8页
Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebr... Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase(MAPK) signaling pathway.We established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa's method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize(LU5),Hegu(LI4),Zusanli(ST36),and Sanyinjiao(SP6) for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 + electroacupuncture group.Terminal deoxynucleotidyl transferase(Td T)-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 + electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 + electroacupuncture group compared with the ischemia/reperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves. 展开更多
关键词 nerve regeneration brain injury ELECTROACUpUNCTURE cell apoptosis cerebral ischemia/reperfusion injury neurological impairment score morphological changes immunohistoehemical assay p38 mitogen-activated protein kinases phosphorylated p38 HIppOCAMpUS neural regeneration
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Physiological roles of mitogen-activated-protein-kinase-activated p38-regulated/activated protein kinase 被引量:8
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作者 Sergiy Kostenko Gianina Dumitriu +1 位作者 Kari Jenssen Lgreid Ugo Moens 《World Journal of Biological Chemistry》 CAS 2011年第5期73-89,共17页
Mitogen-activated protein kinases(MAPKs)are a family of proteins that constitute signaling pathways involved in processes that control gene expression,cell division, cell survival,apoptosis,metabolism,differentiation ... Mitogen-activated protein kinases(MAPKs)are a family of proteins that constitute signaling pathways involved in processes that control gene expression,cell division, cell survival,apoptosis,metabolism,differentiation and motility.The MAPK pathways can be divided into conventional and atypical MAPK pathways.The first group converts a signal into a cellular response through a relay of three consecutive phosphorylation events exerted by MAPK kinase kinases,MAPK kinase,and MAPK.Atypical MAPK pathways are not organized into this three-tiered cascade.MAPK that belongs to both conventional and atypical MAPK pathways can phosphorylate both non-protein kinase substrates and other protein kinases.The latter are referred to as MAPK-activated protein kinases.This review focuses on one such MAPK-activated protein kinase,MAPK-activated protein kinase 5(MK5)or p38-regulated/activated protein kinase(PRAK).This protein is highly conserved throughout the animal kingdom and seems to be the target of both conventional and atypical MAPK pathways.Recent findings on the regulation of the activity and subcellular localization,bona fide interaction partners and physiological roles of MK5/PRAK are discussed. 展开更多
关键词 MITOGEN-ACTIVATED protein KINASE p38- regulated/activated protein KINASE Extracellular signalregulated KINASE protein KINASE A SUBCELLULAR localization phosphorylation protein interaction
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Molecular Characterization of Nonstructural Protein NS38 of Grass Carp Reovirus 被引量:5
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作者 Ling SHAO Chao FAN +1 位作者 Ewa Maj Qin FANG 《Virologica Sinica》 SCIE CAS CSCD 2010年第2期123-129,共7页
Viral nonstructural proteins in both enveloped and non-enveloped viruses play important roles in viral replication. Protein NS38 of Grass carp reovirus (GCRV), has been deduced to be a non-structural protein, and, con... Viral nonstructural proteins in both enveloped and non-enveloped viruses play important roles in viral replication. Protein NS38 of Grass carp reovirus (GCRV), has been deduced to be a non-structural protein, and, consistent with other reoviruses, is considered to cooperate with the NS80 protein in viral particle assembly. To investigate the molecular basis of the role of NS38, a complete protein was expressed in E.coli for the first time. It was found that there is a better expression of NS38 induced with IPTG at 28 ℃ rather than 37 ℃. In addition, the antiserum of NS38 prepared with purified fusion protein and injected into rabbit could be used for detecting NS38 protein expression in GCRV infected cell lysate, while there is not any reaction crossed with purified virus particle, confirming NS38 is not a component of the viral structural protein. The result reported in this study will provide evidence for further viral protein-protein and protein-RNA interaction in dsRNA viruses replication. 展开更多
关键词 Grass carp reovirus (GCRV) Nonstructural protein NS38 Recombinant expression
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Interleukin-1 beta up-regulates tissue inhibitor of matrix metalloproteinase-1 mRNA and phosphorylation of c-jun N-terminal kinase and p38 in hepatic stellate cells 被引量:22
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作者 Ya-Ping Zhang Xi-Xian Yao Xia Zhao 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第9期1392-1396,共5页
AIM: To study the relationship between interleukin-lbeta (IL-1β) up-regulating tissue inhibitor of matrix metalloproteinase-1 (TIMMP-1) mRNA expression and phosphorylation of both c-jun N-terminal kinase (INK)... AIM: To study the relationship between interleukin-lbeta (IL-1β) up-regulating tissue inhibitor of matrix metalloproteinase-1 (TIMMP-1) mRNA expression and phosphorylation of both c-jun N-terminal kinase (INK) and p38 in rat heffatic stellate cells (HSC). METHODS: RT-PCR was performed to measure the expression of TIMMP-1 mRNA in rat HSC. Western blot was performed to measure IL-1β-induced JNK and p38 activities in rat HSC. RESULTS: TIMMP-1 mRNA expression (1.191± 0.079) was much higher after treatment with IL-1β (10 ng/mL) for 24 h than in control group (0.545±0.091) (P〈0.01). IL-1β activated INK and p38 in a time-dependent manner. After stimulation with IL-1β for 0, 5, 15, 30, 60 and 120 min, the INK activity was 0.982±0.299, 1.501±0.720, 2.133±0.882, 3.360±0.452, 2.181±0.789, and 1.385 ± 0.368, respectively. There was a significant difference in JNK activity at 15 min (P〈 0.01), 30 min (P〈 0.01) and 60 min (P〈0.01) in comparison to that at 0 min. The p38 activity was 1.061±0.310, 2.050±0.863, 2.380±0.573, 2.973±0.953, 2.421±0.793, and 1.755 ± 0.433 at the 6 time points (0, 5, 15, 30, 60 and 120 min) respectively. There was a significant difference in p38 activity at 5 min (P〈0.05), 15 min (P〈0.01), 30 min (P〈0.01) and 60 min (P〈0.01) compared to that at 0 min. TIMMP-1 mRNA expression trended to decrease in 3 groups pretreated with different concentrations of SP600125 (10 μmol/L, 1.022±0.113; 20 μmol/L, 0.869±0.070; 40 μmol/L, 0.666±0.123). Their decreases were all significant (P〈0.05, P〈0.01, P〈0.01) in comparison to control group (without SP600125 treatment, 1.163±0.107). In the other 3 groups pretreated with different concentrations of SB203580 (10 μmol/L, 1.507±0.099; 20 μmol/L, 1.698±0.107; 40 μmol/L, 1.857±0.054), the expression of TIMMP-1 mRNA increased. Their levels were higher than those in the control group (without SB203580 treatment, 1.027 ± 0.061) with a significant statistical significance (P〈 0.01). CONCLUSION: IL-1β has a direct action on hepatic fibrosis by up-regulating TIMMP-1 mRNA expression in ratessionin in rate HSC.JNK and p38 mitogen-activated protein kinases (MAPKs) are involved in IL-1β-induced TIMMP-1 gene expression, and play a distinct role in this process, indicating that p38 and .INK pathways cooperatively mediate TIMP-1 mRNA expression in rat HSC. 展开更多
关键词 Up-Regulation Animals ANTHRACENES Blotting Western Cell Line Enzyme Inhibitors IMIDAZOLES INTERLEUKIN-1 JNK Mitogen-Activated protein Kinases Liver Liver Cirrhosis pHOSpHORYLATION pYRIDINES RNA Messenger Rats Reverse Transcriptase polymerase Chain Reaction Signal Transduction Time Factors Tissue Inhibitor of Metalloproteinase-1 p38 Mitogen-Activated protein Kinases
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Neuroprotective mechanisms of rutin for spinal cord injury through anti-oxidation and anti-inflammation and inhibition of p38 mitogen activated protein kinase pathway 被引量:10
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作者 Hong-liang Song Xiang Zhang +5 位作者 Wen-zhao Wang Rong-han Liu Kai Zhao Ming-yuan Liu Wei-ming Gong Bin Ning 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第1期128-134,共7页
Rutin has anti-inflammatory, antioxidant, anti-viral, anti-tumor and immune regulatory effects. However, the neuroprotective effects of rutin in spinal cord injury are unknown. The p38 mitogen activated protein kinase... Rutin has anti-inflammatory, antioxidant, anti-viral, anti-tumor and immune regulatory effects. However, the neuroprotective effects of rutin in spinal cord injury are unknown. The p38 mitogen activated protein kinase (p38 MAPK) pathway is the most important member of the MAPK family that controls inflammation. We assumed that the mechanism of rutin in the repair of spinal cord injury is associated with the inhibition of p38 MAPK pathway. Allen’s method was used to establish a rat model of spinal cord injury. The rat model was intraperitoneally injected with rutin (30 mg/kg) for 3 days. After treatment with rutin, Basso, Beattie and Bresnahan locomotor function scores increased. Water content, tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 levels, p38 MAPK protein expression and caspase-3 and -9 activities in T8–9 spinal cord decreased. Oxidative stress related markers superoxide dismutase and glutathione peroxidase levels increased in peripheral blood. Rutin exerts neuroprotective effect through anti-oxidation, anti-inflammation, anti-apoptosis and inhibition of p38 MAPK pathway. 展开更多
关键词 nerve regeneration spinal cord injury RUTIN oxidative stress antioxidant ANTI-INFLAMMATION p38 mitogen activated protein kinase pathway ANTI-ApOpTOSIS caspase-3 caspase-9 neural regeneration
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Xuebijing alters tumor necrosis factor-alpha, interleukin-1beta and p38 mitogen activated protein kinase content in a rat model of cardiac arrest following cardiopulmonary resuscitation 被引量:2
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作者 Haifeng Li Mingli Sun Yaxin Yu Xiaoliang Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第33期2573-2576,共4页
We established a rat model of cardiac arrest by clamping the endotracheal tube of adult rats at expiration. Twenty-four hours after cardiopulmonary resuscitation, nerve cell injury and expression of tumor necrosis fac... We established a rat model of cardiac arrest by clamping the endotracheal tube of adult rats at expiration. Twenty-four hours after cardiopulmonary resuscitation, nerve cell injury and expression of tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase content were increased. Rats injected with Xuebijing, a Chinese herb compound preparation, exhibited normal cellular structure and morphology, dense neuronal cytoplasm, and decreased tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase expression at 24 hours following cardiopulmonary resuscitation. These data suggest that Xuebijing can attenuate neuronal injury induced by hypoxia and reperfusion during cardiopulmonary resuscitation. 展开更多
关键词 cardiac arrest brain tumor necrosis factor-α INTERLEUKIN-1Β p38 mitogen activated protein kinase XUEBIJING cardiopulmonary resuscitation
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Hippocampal activation of c-Jun N-terminal kinase,protein kinase B,and p38 mitogen-activated protein kinase in a chronic stress rat model of depression 被引量:1
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作者 Wei Dai Weidong Li +2 位作者 Jun Lu Yingge A Ya Tu 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第19期1486-1490,共5页
Recent studies have shown that varied stress stimuli activate c-Jun N-terminal kinase (JNK), protein kinase B (Akt), and p38 mitogen-activated protein kinase (p38) signal transduction pathway, and also regulate ... Recent studies have shown that varied stress stimuli activate c-Jun N-terminal kinase (JNK), protein kinase B (Akt), and p38 mitogen-activated protein kinase (p38) signal transduction pathway, and also regulate various apoptotic cascades. JNK and p38 promote apoptosis, but Akt protects against apoptosis, in hippocampal neurons. However, changes in the transduction pathway in different regions of brain tissues in a chronic stress rat model of depression remain poorly understood. Results from this study showed that JNK phosphorylation levels were significantly greater in the stress group hippocampus compared with the control group (P 〈 0.05). No significant difference in JNK phosphorylation levels was detected in the rat cerebral cortex between stress and control groups, and no significant difference in Akt and p38 phosphorylation levels was detected in the rat hippocampus and cerebral cortex between stress and control groups (P 〉 0.05). These results suggested that the JNK signal pathway is activated by JNK phosphorylation and participates in pathophysiological changes in rat models of depression. 展开更多
关键词 DEpRESSION chronic stress pHOSpHORYLATION stress-activated protein kinase protein kinase B p38 mitogen-activated protein kinase neural regeneration
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Inhibiting p38 mitogen-activated protein kinase attenuates cerebral ischemic injury in Swedish mutant amyloid precursor protein transgenic mice 被引量:1
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作者 Liangyu Zou Haiyan Qin +3 位作者 Yitao He Heming Huang Yi Lu Xiaofan Chu 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第14期1088-1094,共7页
Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase (MAPK) inhibitor $B239063 into Swedish mutant amyloid precursor protein (APP/SW... Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase (MAPK) inhibitor $B239063 into Swedish mutant amyloid precursor protein (APP/SWE) transgenic and non-transgenic mice. The number of surviving neurons in the penumbra was quantified using Nissl staining, and the activity of p38 MAPKs was measured by western blotting. The number of surviving neurons in the penumbra was significantly reduced in APP/SWE transgenic mice compared with non-transgenic controls 7 days after cerebral ischemia, but the activity of p38 MAPKs was significantly elevated compared with the non-ischemic hemisphere in the APP/SWE transgenic mice. SB239063 prevented these changes. The APP/SWE mutation exacerbated ischemic brain injury, and this could be alleviated by inhibiting p38 MAPK activity. 展开更多
关键词 cerebral ischemia amyloid precursor protein TRANSGENIC Alzheimer's disease p38mitogen-activated protein kinase SB239063 neural regeneration
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INVOLVEMENT OF p38 MITOGEN-ACTIVATED PROTEIN KINASE IN E.coli-INDUCED U937 APOPTOSIS 被引量:1
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作者 Jia-he Wang Yi-jun Zhou +1 位作者 Ping He Bai-yi Chen 《Chinese Medical Sciences Journal》 CAS CSCD 2007年第1期49-53,共5页
Objective To investigate whether the effect of E. coli on U937 cell fines apoptosis is mediated via p38 mitogen-activated protein kinase (MAPK) activation. Methods The U937 cell lines were treated with E. coli at d... Objective To investigate whether the effect of E. coli on U937 cell fines apoptosis is mediated via p38 mitogen-activated protein kinase (MAPK) activation. Methods The U937 cell lines were treated with E. coli at different time or together with SB203580, an inhibitor for p38. Cell apoptosis was analyzed by flow cytometry, p38 activities were detected by Western blotting. Results E. coli induced apoptosis in cultured U937 cell lines in a time-dependent manner. The phosphorylation of p38 was induced after 10 minutes infection, reached the peak after 20 minutes, and started to decline after 30 minutes. In contrast, the level of total p38 protein was not changed in whole experimental period. Inhibition of p38 with SB203580 significantly inhibited E. coli induced apoptosis in U937 cells. Conclusion The activation of the p38 MAPK in U937 cell lines by E. coli is a major pathway to mediate the apoptosis. 展开更多
关键词 E. coli ApOpTOSIS U937 p38 mitogen-activated protein kinase
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“Three Methods and Three Points” regulates p38 mitogen-activated protein kinase in the dorsal horn of the spinal cord in a rat model of sciatic nerve injury 被引量:8
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作者 Xin Guo Tian-yuan Yu +8 位作者 Wong Steven Wen-duan Jia Chi Ma Yan-hong Tao Chao Yang Tao-tao Lv Shuai Wu Meng-qian Lu Jia-li Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第12期2018-2024,共7页
Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dor... Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dorsal horn using the Dian, Bo, and Rou method in Yinmen(BL37), Yanglingquan(GB34), and Weizhong(BL40). Treatment prevents muscle atrophy, protects spinal cord neurons, and promotes sciatic nerve repair. The mechanisms of action of tuina for treating peripheral nerve injury remain poorly understood. This study established rat models of sciatic nerve injury using the crushing method. Rats received Chinese tuina in accordance with the principle of "Three Methods and Three Points," once daily for 20 days. Tuina intervention reduced paw withdrawal latency and improved wet weight of the gastrocnemius muscle, as well as promoting morphological recovery of sciatic nerve fibers, Schwann cells, and axons. The protein expression levels of phospho-p38 mitogen-activated protein kinase, tumor necrosis factor-α, and interleukin-1β also decreased. These findings indicate that "Three Methods and Three Points" promoted morphological recovery and improved behavior of rats with peripheral nerve injury. 展开更多
关键词 nerve regeneration tuina Three Methods and Three points phospho-p38 mitogen-activated protein kinase sciatic nerve injury tumor necrosis factor-α interleukin-1β dorsal horn of the spinal cord neural regeneration
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p38 mitogen-activated protein kinase regulates type-Ⅰ vs type-Ⅱ phenotyping of human vascular endothelial cells 被引量:1
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作者 Masako Nakahara Miwako Nishio +2 位作者 Koichi Saeki Akira Yuo Kumiko Saeki 《World Journal of Translational Medicine》 2015年第3期101-112,共12页
AIM: To identify kinases involved in phenotype regulation of vascular endothelial cells(VECs): Proproliferative G-protein signaling 5(RGS5)^(high)(typeⅠ) vs anti-proliferative RGS5^(low)(typeⅡ) VECs.METHODS: Proteom... AIM: To identify kinases involved in phenotype regulation of vascular endothelial cells(VECs): Proproliferative G-protein signaling 5(RGS5)^(high)(typeⅠ) vs anti-proliferative RGS5^(low)(typeⅡ) VECs.METHODS: Proteomic kinase assays were performed to identify the crucial kinase involved in the phenotype regulation of human VECs using typeⅠ VECs, which promotes the proliferation of human vascular smooth muscle cells(VSMCs), and typeⅡ VECs, which suppress the proliferation of human VSMCs. The assays were performed using multiple pairs of typeⅠ and typeⅡ VECs to obtain the least number of candidates. The involvement of the candidate kinases was verified by evaluating the effects of their specific inhibitors on the phenotype regulation of human VECs as well as the expression levels of regulator of RGS5, which is the causative gene for the "typeⅡ to typeⅠ" phenotype conversion of human VECs. RESULTS: p38α mitogen-activated protein kinase(p38α MAPK) was the only kinase that showed distinctive activities between typeⅠ and typeⅡ VECs: p38α MAPK activities were low and high in type-Ⅰand typeⅡ VECs, respectively. We found that an enforced expression of RGS5 indeed lowered p38α MAPK activitiesin typeⅡ VECs. Furthermore, treatments with a p38α MAPK inhibitor nullified the anti-proliferative potential in typeⅡ VECs. Interestingly, MAPK inhibitor treatments enhanced the induction of RGS5 gene. Thus, there is a vicious cycle between "RGS5 induction" and "p38α MAPK inhibition", which can explain the unidirectional process in the stress-induced "typeⅡ to typeⅠ" conversions of human VECs. To understand the upstream signaling of RGS5, which is known as an inhibitory molecule against the G protein-coupled receptor(GPCR)-mediated signaling, we examined the effects of RGS5 overexpression on the signaling events from sphingosine-1-phosphate(S1P) to N-cadherin, because S1 P receptors belong to the GPCR family gene and N-cadherin, one of their downstream effectors, is reportedly involved in the regulation of VEC-VSMC interactions. We found that RGS5 specifically bound with S1P1. Moreover, N-cadherin localization at intercellular junctions in typeⅡ VECs was abolished by "RGS5 overexpression" and "p38α MAPK inhibition".CONCLUSION: p38α MAPK plays crucial roles in "type-Ⅰ vs type-Ⅱ" phenotype regulations of human VECs at the downstream of RGS5. 展开更多
关键词 VASCULAR endothelial CELLS VASCULAR smooth muscle CELLS proteomic KINASE assay p38αmitogenactivated protein KINASE regulator of G-protein signaling 5 sphingosine-1-phosphate N-cadherin
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Cross-talk between Smad4 and P38 Proteins in Non-small Cell Lung Cancer
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作者 童向东 刘宏旭 +4 位作者 赵惠儒 王宇 李玉 韩立波 张林 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2007年第4期269-276,共8页
Objective: Impaired signal transduction is associated with tumorigenesis and progression of various kinds of human cancers. Transforming growth factor (TGF)-beta/Smad and ras-mitogen activated protein kinase (MAPK... Objective: Impaired signal transduction is associated with tumorigenesis and progression of various kinds of human cancers. Transforming growth factor (TGF)-beta/Smad and ras-mitogen activated protein kinase (MAPK) are two major signal transduction pathways for adjusting cell proliferation and differentiation. Little is known about TGF-beta/Smad4 in non-small cell lung cancer (NSCLC). Hereby, we investigated the expression of Smad4 in NSCLC, its correlation with MAPK proteins (including p38, ERK1 and JNK1 proteins) and their clinical significance in NSCLC. Methods: The expressions of Smad4, p38, ERK1 and JNK1 were detected at protein level with Western blotting and immunohistochemistry, at transcription level with RT-PCR. Statistical analysis was performed for the comparisons of expressions of Smad4, p38, ERK1 and JNK1, and their correlation with various clinicopathological parameters and the prognosis of NSCLC. Results: The levels of protein and mRNA expression of Smad4 in lung cancer tissues were significantly lower than in normal tissues (P〈0.05). All these four proteins were associated with TNM staging. There was a strongly negative correlation between p38 and Smad4. Expressions of Smad4, p38 and JNK1, as well as tumor differentiation and staging were significantly correlated with the prognosis of NSCLC by univariate analysis. By multivariate analysis, only Smad4, p38, tumor differentiation and staging were correlated with the prognosis. Taken together, the negative expression of p38 and positive expression of Smad4 were associated with a better prognosis of NSCLC. Conclusion: Smad4 could be of vital importance for the initiation and development of NSCLC. The expression of Smad4 might be inhibited by p38, supporting a cross-talk between main proteins of TGF-beta/Smad and ras-MAPK signal transduction pathways. Smad4 and p38 could be possible prognostic factors for NSCLC. 展开更多
关键词 Signal transduction Non Small Cell Lung Cancer(NSCLC) Smad4 protein Transforming growthfactor-beta Mitogen-activated protein kinase p38 protein JNK1 protein ERK1 protein
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N-methyl-D-aspartate receptor effects on p38 mitogen activated protein kinase and its role in a rat model of diabetic neuropathic pain
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作者 Changbin Ke Xiaoxia Huang +4 位作者 Xianghong Luo Xiancheng Xu Chengming Qin Xianyu Wang Juying Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第11期868-873,共6页
BACKGROUND: Activated N-methyl-D-aspartate (NMDA) receptor is involved in the formation of chronic neuropathic pain, and its antagonist, ketamine, exhibits effective amelioration of diabetic neuropathic pain (DNP... BACKGROUND: Activated N-methyl-D-aspartate (NMDA) receptor is involved in the formation of chronic neuropathic pain, and its antagonist, ketamine, exhibits effective amelioration of diabetic neuropathic pain (DNP). However, the mechanisms of NMDA receptor participation in the formation and maintenance of DNP remain poorly understood. OBJECTIVE: To evaluate the role NMDA receptor plays in DNP and effects on p38 mitogen activated protein kinase (p38 MAPK) in a rat model of DNP. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Human Embryonic Stem Cell Research Institute of Yunyang Medical College Affiliated Taihe Hospital between July 2005 and September 2007. MATERIALS: Streptozotocin was provided by Sigma, USA; p38 MAPK inhibitor (SB203580) was provided by Shanghai KangChen Biotech, China; NMDA receptor antagonist (MK-801) was purchased from Shanghai Yope Biotech, China. METHODS: A total of 128 healthy, Wistar rats of clean grade, aged 3 months and weighing 180- 220 g, were randomly assigned to 4 groups: control, DNP model, p38 MAPK, and NMDA receptor. Each group contained 32 rats. DNP was established in all groups except for the control group by intraperitoneal injection of streptozocin (65 mg/kg). Subsequently, 1 mg/kg SB203580 and 1 mg/kg MK-801 were injected once each week via intraperitoneal injection in the p38 MAPK and NMDA receptor groups, respectively. MAIN OUTCOME MEASURES: At the end of 2, 4, 6, and 8 weeks following streptozotocin injection, mechanical withdrawal threshold was measured in 8 animals from each group following von Frey filament stimulation. The rats were anesthetized and nerve conduction velocity of the left sciatic nerve was measured. Subsequently, the right sciatic nerve, the lumbar segment of the spinal cord, and dorsal root ganglia were removed from the L3-6 segment for microscopic examination, p38 MAPK expression was determined using immunohistochemistry and Western blot analysis. Expression of NMDA receptor 1 mRNA in dorsal root ganglion and spinal cord neurons was detected using RT-PCR. RESULTS: Mechanical withdrawal threshold and nerve conduction velocity were significantly reduced, and p38 MAPK and NMDA receptor 1 mRNA expression in the spinal cord and dorsal root ganglia were significantly increased, in the model, p38 MAPK, and NMDA receptor groups compared with the control group at all time points (P 〈 0.05). At 4-8 weeks following successful DNP model establishment, SB203580 and MK-801 increased mechanical withdrawal threshold, accelerated nerve conduction velocity, and attenuated p38 MAPK expression, compared with the model group. The NMDA receptor group exhibited downregulated mRNA expression of NMDA receptor 1 compared with the model and p38 MAPK groups (P 〈 0.05). CONCLUSION: NMDA receptor was highly expressed in the brains of DNP rats and was involved in DNP development via activation of the p38 MAPK signal pathway. 展开更多
关键词 N-methyI-D-aspartate receptors p38 mitogen-activated protein kinases diabetic neuropathy NEURALGIA
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Functional study of p38 mitogen-activated protein kinase based on cell-penetrating peptide delivery system
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作者 Liping Yang Yongming Yao Zhiyong Sheng Xiaomei Zhu Yong Jiang 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2009年第2期108-114,共7页
Objective p38 Mitogen-activated protein kinase (MAPK) is a crossing center of various pathways. In this study, protein transduction system based on human immunodeficiency virus (HIV)-1 transactivator of transcript... Objective p38 Mitogen-activated protein kinase (MAPK) is a crossing center of various pathways. In this study, protein transduction system based on human immunodeficiency virus (HIV)-1 transactivator of transcription (TAT), which is an efficient delivery peptide of the foreign proteins into cells, was employed to study p38 MAPK functions in eukaryotic cells. Methods p38 And its dominant negative form, p38AF, were constructed into pET-His-TAT vector correctly to verify that the recombinant plasmids were well-founded through restriction enzyme digestion and DNA sequencing. The two proteins, His-TAT-p38 and His-TAT-p38AF, were expressed and purified in Escherichia coli by SDS-PAGE. Then they were incubated with ECV304 cells respectively and readily transduced into cells in a time-dependent and dose-dependent manner. The cells were stimulated by sorbitol. Activating transcription factor (ATF) 2 phosphorylation level was checked using Western blot to assess the activity of endogenous p38. Results Compared with controls, it was found that His-TAT-p38 increased the level ofATF2 phosphorylation in sorbitol-stimulated ECV304 cells, while His-TAT-p38AF inhibited it, indicating p38 MAPK protein delivery system based on TAT was constructed successfully. TAT-p38 and its dominant negative form possessed high biological activity after transduction into ECV304 cells by TAT protein delivery system. The results showed that p38AF fused with TAT could inhibit the transduction of endogenous p38 signal pathway in part, and other pathway might regulate p38 phosphorylation. Conclusions Our study provides a novel pathway to inhibit p38 signal pathway and establish a new method to study p38 function. 展开更多
关键词 Human immunodeficiency virus-1 transactivator of transcription p38 mitogen-activated protein kinase protein transduction: sorbitol
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Role of p38 Mitogen-activated Protein Kinase in Mediating Monocyte Chemoattractant Protein-1 in Human Umbilical Vein Endothelial Cells
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作者 李艳波 邓华聪 +1 位作者 郑丹 李呼伦 《Chinese Medical Sciences Journal》 CAS CSCD 2004年第1期71-71,共1页
关键词 Cells Cultured Endothelial Cells Humans Mitogen-Activated protein Kinases Monocyte Chemoattractant protein-1 RNA Messenger Research Support Non-U.S. Gov't Umbilical Veins p38 Mitogen-Activated protein Kinases
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