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Abrupt changes in fkbp12.6 and SERCA2a expression contribute to sudden occurrence of ventricular fibrillation on reperfusion and are prevented by CPU86017

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Acta Pharmacologica Sinica 2007年第6期28卷 773-782页

作者： Tao NA~2,Zhi-jiang HUANG~2,De-zai DAI~(2,3),Yuan ZHANG~2,Yin DAI~2~2 Research Division of Pharmacology,China Pharmaceutical University,Nanjing 210009,China Research Division of Pharmacology China Pharmaceutical University Nanjing China

Aim:The occurrence of ventricular fibrillation (VF) is dependent on the deteriora-tion of channelopathy in the *** is interesting to investigate molecularchanges in relation to abrupt appearance of VF on *** aimed to studywhether changes in the expression of fkbp12.6 and SERCA2a and the endothelin(ET) system on reperfusion against ischemia were related to the rapid occurrenceof VF and whether CPU86017,a class Ⅲ antiarrhythmic agent which blocks IKr,*** ICa.L,suppressed VF by correcting the molecular changes on ***:Cardiomyopathy (CM) was produced by 0.4 mg/kg sc L-thyroxin for10 d in rats,and subjected to 10 min coronary artery ligation/reperfusion on *** of the Ca2+handling and ET system and calcium transients wereconducted and CPU86017 was injected (4 mg/kg,sc) on d ***:A highincidence of VF was found on reperfusion of the rat CM hearts,but there was noVF before *** elevation of diastolic calcium was significant in theCM myocytes and exhibited abnormality of the Ca2+handling *** rapiddownregulation of mRNA and the protein expression of fkbp12.6 and SERCA2awere found on reperfusion in association with the upregulation of the expressionof the endothelin-converting enzyme (ECE) and protein kinase A (PKA),in contrast,no change in the ryanodine type 2 receptor (RyR2),phospholamban (PLB),endothelin A receptor (ETAR),and iNOS was ***86017 removed thesechanges and suppressed ***:Abrupt changes in the expression offkbp12.6,SERCA2a,PKA,and ECE on reperfusion against ischemia,which areresponsible for the rapid occurrence of VF,have been *** changesare effectively prevented by CPU86017.

关键词： sudden cardiac death ventricular fibrillation endothelin fkbp12.6 SERCA2a protein kinase A CPU86017 cardiomyopathy Lthyroxin endothelin-converting enzyme

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Reversal of isoproterenol-induced downregulation of phospholamban and fkbp12.6 by CPU0213-mediated antagonism of endothelin receptors

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Acta Pharmacologica Sinica 2007年第11期28卷 1746-1754页

作者： Yu FENG,Xiao-yun TANG,De-zai DAI~2,Yin DAIResearch Division of Pharmacology,China Pharmaceutical University,Nanjing 210009,China Research Division of Pharmacology China Pharmaceutical University Nanjing China

Aim:The downregutation of phospholamban (PLB) and fkbp12.6 as a result of β-receptor activation is involved in the pathway(s) of congestive heart *** that the endothelin (ET)-1 system may link to downregulated PLBand ***:Rats were subjected to ischemia/reperfusion (I/R) tocause heart failure (HF).1 mg/kg isoproterenol (ISO) was injected subcutane-ously (sc) for 10 d to worsen HF.30 mg/kg CPU0213 (sc),a dual ET receptor.(ETAR/ETBR) antagonist was given from d 6 to d *** d 11,cardiac function wasassessed together with the determination of mRNA levels of ryanodine receptor 2,calstabin-2 (fkbp12.6),PLB,and sarcoplasmic reticulum Ca2+-*** rat ventricular myocytes were incubated with ISO at 1×10-6mol/L to set up anin vitro model of *** (PRO),CPU0213,and darusentan (DAR,anETAR antagonist) were incubated with cardiomyocytes at 1×10-5mol/L or 1×10-6mol/L in the presence of ISO (1×10-6mol/L).Immunocytochemistry and Westernblotting were applied for measuring the protein levels of PLB and ***:The worsened hemodynamics produced by I/R were exacerbated by *** significant downregulation of the gene expression of PLB andfkbp12.6 and worsened cardiac function by ISO were reversed by *** ISO 1×10-6mol/L produced a sharp decline of PLB and fkbp12.6 proteinsrelative to the *** downregulation of the protein expression was signifi-cantly reversed by the ET receptor antagonist CPU0213 or DAR,comparable tothat achieved by ***:This study demonstrates a role of ET inmediating the downregulation of the cardiac Ca2+-handling protein by ISO.

关键词： heart failure endothelin receptor antagonists phospholamban fkbp12.6 propranolol CPU0213

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fkbp12.6 Knockout Increases Ryanodine Receptors Open Probability During β-adrenergic Stimulation in Mice Cardiac Myocytes

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生物物理学报 2009年第S1期25卷 248-249页

作者： Zhao Yanting1, Zhou Peng1, Chen Zheng2, Ji Guangju2, Wang Shiqiang1 1State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, and 2Institute of Biophysics, Chinese Academy of Sciences, Being, China, 100871

FK506 binding protein 12.6 (fkbp12.6) is the protein in the ryanodine receptor complex, but its function is controversial in different reported work. Some conclude that fkbp12.

关键词： β-adrenergic fkbp12.6 isoproterenol ryanodine receptor spark

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Ca^(2+) Release Induced by cADP-Ribes Is Mediated by fkbp12.6 Proteins in Mouse Bladder Smooth Muscle

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生物物理学报 2009年第S1期25卷 207-208页

作者： Ji Zheng1,Xu Zhang2, Jinhong Pan1,Bin Wei2, Bo Song1 and Guangju Ji2 1 Urological Surgery Research Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.2 National Laboratory of Biomacromolecules,Institute of Biophysics of Chinese Academy of Sciences, 15 Datun Rd, Beijing 100101, China

Ca2+ release through ryanodine receptors (RyRs) plays an important role in excitation-contraction coupling in heart and smooth muscle. fkbp12.6 proteins

关键词： cADP robes Ca2+ spark fkbp12.6 proteins smooth muscle

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Insulin/PI3K/AKt Signaling Pathway Mediates Cardiac Hypertrophy in fkbp12.6 Deficient Male Mice

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生物物理学报 2009年第S1期25卷 206-207页

作者： Zheng Chen, Zheng-Zheng Li, Wen-Xuan Yin, Guangju Ji Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang District, Beijing 100101

Male mice deficient in fkbp12.6 display cardiac hypertrophy, but the underlying mechanism is still unclear. Here we report that the cardiac hypertrophy is a physiological response

关键词： AKT, insulin cardiac hypertrophy male fkbp12.6 null mice

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fkbp12.6 Knockout Increases Ryanodine Receptors Open Probability During β-adrenergic Stimulation in Mice Cardiac Myocytes

FKBP12.6 Knockout Increases Ryanodine Receptors Open Probabi...

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第十一次中国生物物理学术大会暨第九届全国会员代表大会

作者： Zhao Yanting1,Zhou Peng 1,Chen Zheng 2,Ji Guangju 2,Wang Shiqiang 1 1State Key Laboratory of Biomembrane and Membrane Biotechnology,College of Life Sciences,Peking University,and 2Institute of Biophysics,Chinese Academy of Sciences,Being,China,100871

＜正＞FK506 binding protein 12.6（fkbp12.6）is the protein in the ryanodine receptor complex,but its function is controversial in different reported *** conclude that fkbp12.6

关键词： β-adrenergic fkbp12.6 isoproterenol ryanodine receptor spark

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fkbp12.6重组腺病毒载体的构建及其心肌细胞感染效率测定

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中山大学学报（医学科学版） 2006年第3期27卷 271-275页

作者：李德伍卫周淑娴中山大学附属第二医院心内科广东广州510120

目的构建携带fkbp12.6基因的重组腺病毒载体以研究fkbp12.6在心力衰竭时心室肌电重构中的作用。方法将平端化的fkbp12.6片段连接到穿梭质粒pAdTrack-CMV构建重组穿梭质粒pAdTrack/fkbp12.6,用XhoI单酶切进行鉴定。采用电穿孔法将线性化p... 详细信息

目的构建携带fkbp12.6基因的重组腺病毒载体以研究fkbp12.6在心力衰竭时心室肌电重构中的作用。方法将平端化的fkbp12.6片段连接到穿梭质粒pAdTrack-CMV构建重组穿梭质粒pAdTrack/fkbp12.6,用XhoI单酶切进行鉴定。采用电穿孔法将线性化pAdTrack/fkbp12.6转化AdEasier-1细菌,产生重组腺病毒质粒pAdEasy-1/fkbp12.6。采用脂质体介导法用线性化pAdEasy-1/fkbp12.6转染293细胞,从病变的293细胞分离、纯化重组腺病毒***12.6;采用PCR方法对其进行鉴定。用重组腺病毒感染乳鼠心肌细胞,在荧光显微镜下计算GFP阳性细胞百分率。结果在病变293细胞的冻融上清中含有重组腺病毒***12.6,其滴度为1.5×1012pfu/mL。当感染复数(MOI)为75时,感染效率可达100%。结论成功构建了携带fkbp12.6基因的重组腺病毒载体;***12.6可高效感染乳鼠心肌细胞。本研究为进一步探讨fkbp12.6在心力衰竭时心室肌电重构中的作用奠定了基础。

关键词： fkbp12.6 腺病毒载体心肌细胞

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fkbp12.6 knockout affect ADP-ribosyl cyclase expression and function of hippocampus in mice

FKBP12.6 knockout affect ADP-ribosyl cyclase expression and ...

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2012国际生理学学术大会

作者： Yuming Li Haitao Li Yanzhi Zhao Yanqiu Cui Junya Wang Dongmei Zhang Zhongqiu Li Department of Physiology and Pathophysiology Capital Medical University Yanjing Medical College

fkbp12.6 and cADPR are two regulators of ryanodine Ca release receptors which play a pivotal role in the regulation of numerous cellular *** current study was designed to examine the effect of fkbp12.6 and ADP-ribosyl cyclase(ADPRclase,a key regulator of endogenous cADPR production) on the function of *** this study,both fkbp12.6 knockout and wild 129 mice(8-12 week old) were divided into three groups respectively:control group,mice were given a 7 day continuous infusion of 0.9%NaCl;DHAB group,mice were given a 7 day continuous infusion of 2,2’-dihydroxyazobenzene(DHAB,a ADPRclase inhibitor,2 mg/***);cADPR group,mice were given a 7 day continuous infusion of exogenous cADPR(1 mg/***) *** the 7th day,abilities of learning and memory of the mice were tested by using the Morris water maze and space *** expression ofADPRclase mRNA and protein in hippocampus of mice were detected by using RT-PCR and Western Blotting *** Morris water maze and space experiments revealed that the abilities of learning and memory were decreased significantly in fkbp 12.6 knockout mice and DHAB treated wild 129 *** abilities decrease was aggravated by DHAB and alleviated by exogenous cADPR in fkbp12.6 knockout *** of mRNA and protein of ADPRclase was lower in fkbp12.6 knockout mice than that in wild *** inhibited the expression of ADPRclase in both fkbp12.6 knockout and wild *** data shows that ADPRclase expression was decreased by fkbp12.6 knockout and fkbp 12.6/ADPRclase/cADPR may maintain the function of hippocampus in mice.

关键词： fkbp12.6 ADP-ribosyl cyclase hippocampus

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fkbp12.6 plays a vital role in regulating hippocampal neuron signaling in mice

FKBP12.6 plays a vital role in regulating hippocampal neuron...

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第十七届国际生物物理大会;第十二届中国生物物理大会

作者： Shaopeng Chi,Qi Yuan,Yanyun Wu,Guangiu Ji National Laboratory of Biomacromolecules,Institute of Biophysics,Chinese Academy of Sciences,15 Datun Road,Chaoyang District,Beijing 100101,China.

As has been known that hippocamp plays a major role in learning and *** studies indicate that intracellular calcium release channel ryanodine receptor isoform 2(RyR2) is richly expressed in CA3 and Dentate gyrus areas in hippocamp and plays an important role in memory and spatial learning *** like ***12 which associates with RYRl,protein fkbp12.6 more selectively associates with RYR2 which

关键词： fkbp12.6 memory and motility behaviors hippocampal neurons apoptosis

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fkbp12.6基因转染对心衰犬心功能及心肌病理变化的影响

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第三军医大学学报 2008年第5期30卷 431-434页

作者：王逵杨成明刘国通王旭开曾春雨王红勇方玉强傅春江石伟彬第三军医大学大坪医院野战外科研究所心血管内科重庆400042

目的探讨白蛋白微泡介导的pcDNA3.1-fkbp12.6质粒转染对心衰犬心功能及心肌病理变化的影响。方法28只快速起搏心衰犬分为2组。转染组以白蛋白微泡为载体,在超声破坏下将人工合成的pcDNA3.1-fkbp12.6质粒转染入心肌,以不含质粒的微泡作... 详细信息

目的探讨白蛋白微泡介导的pcDNA3.1-fkbp12.6质粒转染对心衰犬心功能及心肌病理变化的影响。方法28只快速起搏心衰犬分为2组。转染组以白蛋白微泡为载体,在超声破坏下将人工合成的pcDNA3.1-fkbp12.6质粒转染入心肌,以不含质粒的微泡作为对照组。两组又分为转染后4d(转染Ⅰ组)和14d(转染Ⅱ组)。分别在起搏器安置前、转染前、转染后,采用超声测量左室内径、心功能评价fkbp12.6基因对心衰的治疗效果。通过HE染色和透射电镜观察心肌病理变化。应用RT-PCR检测各组fkbp12.6基因的表达情况。结果超声微泡介导的转染可以提高心肌fkbp12.6 mRNA的表达。心肌病理显示转染组病变轻于对照组,而且未转染组病变进一步恶化。转染组EF、FS在第4天可见明显好转,并在14d时保持稳定,但一直低于正常水平。在第4天时转染组LVEDD与对照组无变化,而LVEDV下降(P=0.04),在14d时两指标与对照组比较均缩小(LVEDD和LVEDV的P值分别为0.012和0.005)。结论通过超声微泡介导转染fkbp12.6基因可以改善心脏功能,逆转心肌重塑,减轻心肌病理变化。

关键词：心力衰竭 fkbp12.6 基因治疗心功能病理学

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