Perilipin1(PLIN1)is a major phosphorylated protein that specifically coats the surface of neutral lipid droplets(LDs)in adipocytes and plays a crucial role in regulating the accumulation and hydrolysis of triacylglyce...Perilipin1(PLIN1)is a major phosphorylated protein that specifically coats the surface of neutral lipid droplets(LDs)in adipocytes and plays a crucial role in regulating the accumulation and hydrolysis of triacylglycerol(TG).Mammalian studies have shown that Plin1 gene transcription is mainly regulated by peroxisome proliferator-activated receptorgamma(PPARγ),the master regulator of adipogenesis.However,the regulatory mechanism of the chicken Plin1(c Plin1)gene is poorly understood.The present study aimed to investigate whether Plin1 is regulated by PPARγin chickens and identify its exact molecular mechanism.Reporter gene and expression assays showed that PPARγ2,but not PPARγ1,activated(P<0.01)the cPlin1 gene promoter.An electrophoretic mobility shift assay and mutational analysis revealed that PPARγ2 bound to a special site in the cPlin1 gene promoter to enhance its expression.In summary,our results show that PPARγpromotes the expression of the cPlin1 gene and that PPARγ2 is the main regulatory isoform.展开更多
In gliomas, the canonical Wingless/Int（WNT）/b-catenin pathway is increased while peroxisome proliferator-activated receptor gamma（PPAR-c） is downregulated.The two systems act in an opposite manner. This review foc...In gliomas, the canonical Wingless/Int（WNT）/b-catenin pathway is increased while peroxisome proliferator-activated receptor gamma（PPAR-c） is downregulated.The two systems act in an opposite manner. This review focuses on the interplay between WNT/b-catenin signaling and PPAR-c and their metabolic implications as potential therapeutic target in gliomas. Activation of the WNT/bcatenin pathway stimulates the transcription of genes involved in proliferation, invasion, nucleotide synthesis,tumor growth, and angiogenesis. Activation of PPAR-c agonists inhibits various signaling pathways such as the JAK/STAT, WNT/b-catenin, and PI3 K/Akt pathways,which reduces tumor growth, cell proliferation, cell invasiveness, and angiogenesis. Nonsteroidal anti-inflammatory drugs, curcumin, antipsychotic drugs, adiponectin,and sulforaphane downregulate the WNT/b-catenin pathway through the upregulation of PPAR-c and thus appear to provide an interesting therapeutic approach for gliomas.Temozolomide（TMZ） is an antiangiogenic agent. The downstream action of this opposite interplay may explain the TMZ-resistance often reported in gliomas.展开更多
Objective： To investigate the expressions of GSK-3beta, Beta-catenin and PPAR-gamma, and their relationship in medulloblastoma, and to explore their value in clinic application. Methods： Immunohistochemical stainin...Objective： To investigate the expressions of GSK-3beta, Beta-catenin and PPAR-gamma, and their relationship in medulloblastoma, and to explore their value in clinic application. Methods： Immunohistochemical staining with SP method was conducted to determine the expressions of GSK-3beta, Beta-catenin and PPAR-gamma in 48 cases of medulloblastoma and 10 normal cerebellar tissues. Results： The rate of abnormal expressions of beta-catenin and PPAR-gamma in MB was higher than that in normal. Conversely, GSK-3beta in MB was lower than that in the normal （P〈0.05）. Furthermore, in medulloblastoma, beta-catenin and GSK-3beta showed a negative correlation, PPAR-gamma and beta-catenin had a positive correlation. Conclusion： Abnormal expression of beta-catenin plays a crucial role in the development of medulloblastoma. Meanwhile, PPAR-gamma and GSK-3beta which are tightly related with beta-catenin are both involved in the genesis and development of medulloblastoma.展开更多
目的检测过氧化物酶体增殖激活性受体γ(PPARγ)在肝癌组织中有无差异性表达且有无突变。方法用半定量RT- PCR,Western blot,FISH,PCR-SSCP等方法进行鉴定。结果用半定量RT-PCR检测,有8/14为癌中高表达;Western blot 方法检测,9/15为癌...目的检测过氧化物酶体增殖激活性受体γ(PPARγ)在肝癌组织中有无差异性表达且有无突变。方法用半定量RT- PCR,Western blot,FISH,PCR-SSCP等方法进行鉴定。结果用半定量RT-PCR检测,有8/14为癌中高表达;Western blot 方法检测,9/15为癌中高表达。免疫组化显示PPARγ在所有的癌旁组织中定位于细胞浆中;而在5个癌组织中定位于细胞核中;突变热点PPARγ外显子3和5在34对肝癌标本中没有突变。结论过氧化物酶体增殖激活性受体γ在肝癌组织中有差异性表达并且在肝癌标本中没有突变。提示PPARγ可能与肝癌的发展有一定的相关性。展开更多
目的探讨PPARγ上调miR-16的机制及其抑制脓毒症炎症反应的作用。方法经Real time RT-PCR检测脓毒症患者和健康者的外周血单核细胞PPARγ和miR-16的表达,分析其相关性;分别用PPARγ激动剂RGZ、PPARγsiRNA或miR-16抑制剂(antagomir-16)...目的探讨PPARγ上调miR-16的机制及其抑制脓毒症炎症反应的作用。方法经Real time RT-PCR检测脓毒症患者和健康者的外周血单核细胞PPARγ和miR-16的表达,分析其相关性;分别用PPARγ激动剂RGZ、PPARγsiRNA或miR-16抑制剂(antagomir-16)处理THP-1和RAW246.7,经real time RT-PCR和Western blot检测miR-16及其靶基因IKKα的表达;细胞转染含miR-16启动子的报告基因质粒,经PPARγ激动剂RGZ或拮抗剂GW9662处理后,检测细胞报告基因活性;细胞经PPARγ激动剂RGZ处理,再经LPS处理,ELISA检测炎症因子TNFα和IL-6的表达;LPS诱导的脓毒症小鼠经PPARγ激动剂RGZ,或经antagomir-16预处理后,再经PPARγ激动剂RGZ处理小鼠,real time RT-PCR检测小鼠外周血单核细胞中miR-16的表达,ELISA检测血清炎症因子TNFα和IL-6的表达。结果脓毒症患者外周血单核细胞中PPARγ与miR-16的表达均降低且二者的表达呈显著负相关(P<0.05);PPARγ通过促进miR-16的启动子活性上调miR-16的表达,进而抑制miR-16靶分子IKKα的表达(P<0.05);PPARγ上调miR-16后显著抑制炎症细胞产生TNFα和IL-6(P<0.05);PPARγ上调miR-16抑制脓毒症小鼠血清TNFα和IL-6的表达(P<0.05)。结论激动剂活化的PPARγ上调miR-16进而抑制细胞炎症因子表达及脓毒症小鼠炎症反应。展开更多
基金supported by the National Natural Science Foundation of China(31201796 and 32072704)the China Agriculture Research System of MOF and MARA(CARS-41)the Natural Science Foundation of Heilongjiang Province,China(LH2020C017)。
文摘Perilipin1(PLIN1)is a major phosphorylated protein that specifically coats the surface of neutral lipid droplets(LDs)in adipocytes and plays a crucial role in regulating the accumulation and hydrolysis of triacylglycerol(TG).Mammalian studies have shown that Plin1 gene transcription is mainly regulated by peroxisome proliferator-activated receptorgamma(PPARγ),the master regulator of adipogenesis.However,the regulatory mechanism of the chicken Plin1(c Plin1)gene is poorly understood.The present study aimed to investigate whether Plin1 is regulated by PPARγin chickens and identify its exact molecular mechanism.Reporter gene and expression assays showed that PPARγ2,but not PPARγ1,activated(P<0.01)the cPlin1 gene promoter.An electrophoretic mobility shift assay and mutational analysis revealed that PPARγ2 bound to a special site in the cPlin1 gene promoter to enhance its expression.In summary,our results show that PPARγpromotes the expression of the cPlin1 gene and that PPARγ2 is the main regulatory isoform.
文摘In gliomas, the canonical Wingless/Int（WNT）/b-catenin pathway is increased while peroxisome proliferator-activated receptor gamma（PPAR-c） is downregulated.The two systems act in an opposite manner. This review focuses on the interplay between WNT/b-catenin signaling and PPAR-c and their metabolic implications as potential therapeutic target in gliomas. Activation of the WNT/bcatenin pathway stimulates the transcription of genes involved in proliferation, invasion, nucleotide synthesis,tumor growth, and angiogenesis. Activation of PPAR-c agonists inhibits various signaling pathways such as the JAK/STAT, WNT/b-catenin, and PI3 K/Akt pathways,which reduces tumor growth, cell proliferation, cell invasiveness, and angiogenesis. Nonsteroidal anti-inflammatory drugs, curcumin, antipsychotic drugs, adiponectin,and sulforaphane downregulate the WNT/b-catenin pathway through the upregulation of PPAR-c and thus appear to provide an interesting therapeutic approach for gliomas.Temozolomide（TMZ） is an antiangiogenic agent. The downstream action of this opposite interplay may explain the TMZ-resistance often reported in gliomas.
文摘Objective： To investigate the expressions of GSK-3beta, Beta-catenin and PPAR-gamma, and their relationship in medulloblastoma, and to explore their value in clinic application. Methods： Immunohistochemical staining with SP method was conducted to determine the expressions of GSK-3beta, Beta-catenin and PPAR-gamma in 48 cases of medulloblastoma and 10 normal cerebellar tissues. Results： The rate of abnormal expressions of beta-catenin and PPAR-gamma in MB was higher than that in normal. Conversely, GSK-3beta in MB was lower than that in the normal （P〈0.05）. Furthermore, in medulloblastoma, beta-catenin and GSK-3beta showed a negative correlation, PPAR-gamma and beta-catenin had a positive correlation. Conclusion： Abnormal expression of beta-catenin plays a crucial role in the development of medulloblastoma. Meanwhile, PPAR-gamma and GSK-3beta which are tightly related with beta-catenin are both involved in the genesis and development of medulloblastoma.
文摘目的检测过氧化物酶体增殖激活性受体γ(PPARγ)在肝癌组织中有无差异性表达且有无突变。方法用半定量RT- PCR,Western blot,FISH,PCR-SSCP等方法进行鉴定。结果用半定量RT-PCR检测,有8/14为癌中高表达;Western blot 方法检测,9/15为癌中高表达。免疫组化显示PPARγ在所有的癌旁组织中定位于细胞浆中;而在5个癌组织中定位于细胞核中;突变热点PPARγ外显子3和5在34对肝癌标本中没有突变。结论过氧化物酶体增殖激活性受体γ在肝癌组织中有差异性表达并且在肝癌标本中没有突变。提示PPARγ可能与肝癌的发展有一定的相关性。
文摘目的探讨PPARγ上调miR-16的机制及其抑制脓毒症炎症反应的作用。方法经Real time RT-PCR检测脓毒症患者和健康者的外周血单核细胞PPARγ和miR-16的表达,分析其相关性;分别用PPARγ激动剂RGZ、PPARγsiRNA或miR-16抑制剂(antagomir-16)处理THP-1和RAW246.7,经real time RT-PCR和Western blot检测miR-16及其靶基因IKKα的表达;细胞转染含miR-16启动子的报告基因质粒,经PPARγ激动剂RGZ或拮抗剂GW9662处理后,检测细胞报告基因活性;细胞经PPARγ激动剂RGZ处理,再经LPS处理,ELISA检测炎症因子TNFα和IL-6的表达;LPS诱导的脓毒症小鼠经PPARγ激动剂RGZ,或经antagomir-16预处理后,再经PPARγ激动剂RGZ处理小鼠,real time RT-PCR检测小鼠外周血单核细胞中miR-16的表达,ELISA检测血清炎症因子TNFα和IL-6的表达。结果脓毒症患者外周血单核细胞中PPARγ与miR-16的表达均降低且二者的表达呈显著负相关(P<0.05);PPARγ通过促进miR-16的启动子活性上调miR-16的表达,进而抑制miR-16靶分子IKKα的表达(P<0.05);PPARγ上调miR-16后显著抑制炎症细胞产生TNFα和IL-6(P<0.05);PPARγ上调miR-16抑制脓毒症小鼠血清TNFα和IL-6的表达(P<0.05)。结论激动剂活化的PPARγ上调miR-16进而抑制细胞炎症因子表达及脓毒症小鼠炎症反应。
