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Amelioration of mitochondrial dysfunction in heart failure through S-sulfhydration of Ca^2+/calmodulin-dependent protein kinase Ⅱ
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作者 Dan WU Qing-xun HU +1 位作者 De-qiu ZHU Yi-zhun ZHU 《中国药理学与毒理学杂志》 CSCD 北大核心 2017年第10期976-976,共1页
OBJECTIVE To determine the functional role of hydrogen sulfide(H_2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca^(2+)/calmodulin-dependent protein kinaseⅡ(Ca MKⅡ) us... OBJECTIVE To determine the functional role of hydrogen sulfide(H_2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca^(2+)/calmodulin-dependent protein kinaseⅡ(Ca MKⅡ) using wild type and CSE knockout mouse models.METHODS Continuous subcutaneous injection isoprenaline(7.5 mg·kg^(-1) per day),once a day for 4 weeks to induce heart failure in male C57BL/6(6-8 weeks old) mice and CSE-/-mice.150 μmol·L^(-1) H_2O_2 was used to induce oxidative stress in H9c2 cells.Echocardiograph was used to detect cardiac parameters.H&E stain and Masson stain was to observation histopathological changes.Western blot was used to detect protein expression and activity.The si RNA was used to silence protein expression.HPLC was used to detect H_2S level.Biotin assay was used to detect the level of S-sulfhydration protein.RESULTS Treatment with S-propyl-L-cysteine(SPRC) or sodium hydrosulfide(Na HS),modulators of blood H_2S levels,attenuated the development of heart failure in animals,reduced lipid peroxidation,and preserved mitochondrial function.The inhibition Ca MKⅡ phosphorylation by SPRC and Na HS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds.Interestingly,Ca MKⅡ activity was found to be elevated in CSE-/-mice as compared to wild type animals and the phosphorylation status of Ca MK Ⅱ appeared to relate to the severity of heart failure.Importantly,in wild type mice SPRC was found to promote S-sulfhydration of Ca MKⅡ leading to reduced activity of this protein however,in CSE-/-mice S-sulfhydration was abolished following SPRC treatment.CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of Ca MKⅡ is presented.SPRC mediated S-sulfhydration of Ca MKⅡ was found to inhibit Ca MKⅡ activity and to preserve cardiovascular homeostasis. 展开更多
关键词 hydrogen sulfide MITOCHONDRIA heart failure Ca2+/calmodulin-dependent protein kinase S sulfhydration
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Decorin Induces Cardiac Hypertrophy by Regulating the CaMKⅡ/MEF-2 Signaling Pathway In Vivo 被引量:3
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作者 Yan YANG Wei-wei YU +1 位作者 Wen YAN Qin XIA 《Current Medical Science》 SCIE CAS 2021年第5期857-862,共6页
Objective:Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading,but continuous cardiac hypertrophy can lead to cardiac remodeling and heart failure.Cardiac hypertrophy is mostly consider... Objective:Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading,but continuous cardiac hypertrophy can lead to cardiac remodeling and heart failure.Cardiac hypertrophy is mostly considered reversible,and recent studies have indicated that decorin not only prevents cardiac fibrosis associated with hypertension,but also achieves therapeutic effects by blocking fibrosis-related signaling pathways.However,the mechanism of action of decorin remains unknown and unconfirmed.Methods:We determined the degree of myocardial hypertrophy by measuring the ratios of the heart weight/body weight and left ventricular weight/body weight,histological analysis and immunohistochemistry.Western blotting was performed to detect the expression levels of CaMKⅡ,p-CaMKⅡ and MEF-2 in the heart.Results:Our results confirmed that decorin can regulate the CaMKⅡ/MEF-2 signaling pathway,with inhibition thereof being similar to that of decorin in reducing cardiac hypertrophy.Conclusion:Taken together,the results of the present study showed that decorin induced cardiac hypertrophy by regulating the CaMKⅡ/MEF-2 signaling pathway in vivo,revealing a new therapeutic approach for the prevention of cardiac hypertrophy. 展开更多
关键词 DECORIN cardiac hypertrophy calcium/calmodulin-dependent protein kinase myocyte enhancer factor 2 atrial natriuretic peptide
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Cloning and Characterization of a Homologous Ca^(2+)/Calmodulin-Dependent Protein Kinase PSKH1 from Pearl Oyster Pinctada fucata
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作者 戴益平 谢莉萍 +3 位作者 熊训浩 陈蕾 范为民 张荣庆 《Tsinghua Science and Technology》 SCIE EI CAS 2005年第4期504-511,共8页
Many of the effects of Ca^2+ signaling are mediated through the Ca^2+/calmodulin complex and its acceptors, the Ca^2+/calmodulin-dependent protein kinases, including PSKHI. Studies of the proteins involved in the c... Many of the effects of Ca^2+ signaling are mediated through the Ca^2+/calmodulin complex and its acceptors, the Ca^2+/calmodulin-dependent protein kinases, including PSKHI. Studies of the proteins involved in the calcium metabolism in oysters will help elucidate the pearl formation mechanism. This paper describes a full-length PSKH1 cDNA isolated from pearl oyster Pinctada fucata. Oyster PSKH1 shares 65% homology with human PSKH1 and 48% similarity with rat CaM kinase I in the amino acid sequence, and contains a calmodulin-binding domain. The results of semi-quantitative reverse transcription-polymerase chain reaction and in situ hybridization revealed that oyster PSKH1 mRNA is highly expressed in the outer epithelial cells of the mantle pallial and in the gill epithelial cells. These studies provide important information describing the complex Ca^2+ signaling mechanism in oyster calcium metabolism. 展开更多
关键词 PSKH1 calcium metabolism BIOMINERALIZATION pearl oyster Pinctada fucata Ca^2+/calmodulin-dependent protein kinases (camks)
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心力衰竭大鼠心肌β_3肾上腺素受体表达及其对钙离子相关调节蛋白的作用 被引量:3
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作者 孔一慧 刘玉冰 +2 位作者 张莉 邵群 李悦 《中国老年学杂志》 CAS CSCD 北大核心 2010年第15期2141-2144,共4页
目的研究心力衰竭(HF)大鼠心肌β3肾上腺素受体(beta3-adrenergic receptors,β3-AR)表达情况及对钙离子相关调节蛋白的作用。方法以正常大鼠作对照组,皮下注射生理盐水;实验组大鼠皮下注射异丙肾上腺素(Isoproterenol,ISO),常规饲养8w... 目的研究心力衰竭(HF)大鼠心肌β3肾上腺素受体(beta3-adrenergic receptors,β3-AR)表达情况及对钙离子相关调节蛋白的作用。方法以正常大鼠作对照组,皮下注射生理盐水;实验组大鼠皮下注射异丙肾上腺素(Isoproterenol,ISO),常规饲养8w。造模成功后实验组随机分为3组,激动剂组给予尾静脉注射β3-AR激动剂BRL37344,抑制剂组给予尾静脉注射β3-AR抑制剂SR59230A,HF组给予生理盐水。用药8w后行心脏彩超、RT-PCR法检测心肌组织钙调蛋白(CaM)、钙调蛋白激酶Ⅱ(CaMKⅡ)、肌内质网Ca2+-ATP酶异构体2a(SERCA2a)的mRNA表达。结果①HF组较对照组β3-ARmRNA表达水平增高,CaM、CaMKⅡ、SERCA2amRNA表达水平减低(均P<0.05)。②与HF组相比较,激动剂组β3-ARmRNA水平表达增加,CaM、CaMKⅡ、SERCA2a表达进一步减少(均P<0.05)。③抑制剂组β3-ARmRNA表达水平较对照组减少,CaM、CaMKⅡ、SERCA2a较对照组减低,但较HF组增加(均P<0.05)。结论β3-AR激动剂减低衰竭心肌CaM、CaMKⅡ、SERCA2a的mRNA表达,导致心功恶化,β3-AR抑制剂则相反,可延缓HF进展,预示β3-AR抑制剂在药物治疗HF中的应用前景。 展开更多
关键词 心力衰竭 Calmodulin(CaM) Ca2+/calmodulin-dependent protein kinase camk Sarco/endoplasmic reticulum Ca2+ATPase type 2a(SERCA2a) Β3肾上腺素受体
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鞘内注射KN93对小鼠神经病理性疼痛的镇痛效应 被引量:1
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作者 罗放 田玉科 《临床麻醉学杂志》 CAS CSCD 北大核心 2009年第3期239-241,共3页
目的探讨钙离子/钙调蛋白依赖蛋白激酶Ⅱ(CaMKⅡ)在神经病理性疼痛发病机制中的作用。方法雄性ICR小鼠32只,随机均分为四组:神经病理性疼痛(SNL)组,制作L5/6脊神经结扎(SNL)模型;SNL/KN92组,制作SNL模型,鞘内注射无药理活性的KN93的结... 目的探讨钙离子/钙调蛋白依赖蛋白激酶Ⅱ(CaMKⅡ)在神经病理性疼痛发病机制中的作用。方法雄性ICR小鼠32只,随机均分为四组:神经病理性疼痛(SNL)组,制作L5/6脊神经结扎(SNL)模型;SNL/KN92组,制作SNL模型,鞘内注射无药理活性的KN93的结构类似物KN9245nmol;SNL/KN93组,制作SNL模型,鞘内注射KN9345nmol;假手术(Sham)组,仅显露脊神经而不结扎。分别于SNL术前及术后2~5d每天测定小鼠的机械痛阈和热痛阈,SNL/KN92组与SNL/KN93组于术后5d痛阈测定前30min行鞘内给药。于最后一次痛阈测定毕处死小鼠,取腰段脊髓组织用Western blot检测pCaMKⅡα的表达水平。结果SNL可导致机械痛阈和热痛阈降低(P<0.05),脊髓组织pCaMKⅡα的表达增加(P<0.05);鞘内注射KN93可翻转SNL所致的上述改变(P<0.05),但KN92无此效应。结论CaMKⅡ参与了SNL诱导的神经病理性疼痛的维持,靶向于CaMKⅡ信号途径的治疗可为慢性疼痛治疗提供新的策略。 展开更多
关键词 钙离子 钙调蛋白依赖蛋白激酶 神经痛 临床分析
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1,25二羟维生素D_3通过ERK5通路调节破骨细胞分化 被引量:5
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作者 李忠浩 闫亮 +3 位作者 万浪 丁宁 杨全增 夏亚一 《中国矫形外科杂志》 CAS CSCD 北大核心 2018年第14期1311-1316,共6页
[目的]探讨体外1,25二羟维生素D_3(1,25-(OH)_2-VitD_3)通过细胞外信号调节激酶5(extracellularregulated kinase 5,ERK5)信号通路在诱导破骨细胞分化中的作用。[方法]对骨髓来源巨噬细胞(bone marrow macrophages,BMMs)进行不同浓度(0,... [目的]探讨体外1,25二羟维生素D_3(1,25-(OH)_2-VitD_3)通过细胞外信号调节激酶5(extracellularregulated kinase 5,ERK5)信号通路在诱导破骨细胞分化中的作用。[方法]对骨髓来源巨噬细胞(bone marrow macrophages,BMMs)进行不同浓度(0,10^(-9),10^(-8),10^(-7)mol/L)1,25-(OH)_2-VitD_3孵育,明确1,25-(OH)_2-VitD_3能否激活ERK5信号通路,并筛选出合适浓度的1,25-(OH)_2-VitD_3激活ERK5。调配不同工作液,分为正常细胞对照组、XMD8-92组、1,25-(OH)_2-VitD_3组及1,25-(OH)_2-VitD_3+XMD8-92组,分别孵育BMMs细胞6 d。采用TRAP染色检测4组破骨细胞的分化水平;Western Blot分别检测p-ERK5、ERK5等蛋白水平变化;RT-PCR检测NFATc1、CAMKⅡmRNA相对表达量。[结果]10^(-8)mol/L的1,25-(OH)_2-VitD_3可显著激活ERK5磷酸化(P<0.05)并通过ERK5通路促进破骨细胞分化(P<0.01),但此效应可被ERK5高选择性抑制剂XMD8-92抑制(P<0.05)。ERK5激活可显著上调破骨细胞CAMKⅡ、NFATc1 mRNA的表达(P<0.01);而XMD8-92可显著抑制CAMKⅡm RNA的表达(P<0.01),但对NFATc1 mRNA无显著影响(P>0.05)。[结论]体外低浓度(10^(-8)mol/L)的1,25-(OH)_2-VitD_3通过激活ERK5信号通路促进破骨细胞分化,CAMKⅡ是破骨细胞中ERK5信号下游通路的重要靶点。 展开更多
关键词 1 25二羟维生素D3 细胞外信号调节激酶5 钙调蛋白依赖性蛋白激酶 破骨细胞 分化
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