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Cholesterol metabolic enzyme Ggpps regulates epicardium development and ventricular wall architecture integrity in mice

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Journal of Molecular Cell Biology 2021年第6期13卷 445-454页

作者： Feng Zheng Zhong Chen Qiao-Li Tang Xin-Ying Wang Dan-Yang Chong Tong-Yu Zhang Ya-Yun Gu Zhi-Bin Hu Chao-Jun Li Model Animal Research Centre National Resource Centre for Mutant MiceMedical School of Nanjing UniversityNanjing 210093China State Key Laboratory of Reproductive Medicine Centre for Global HealthSchool of Public HealthNanjing Medical UniversityNanjing 211100China

During embryonic heart development,the progenitor cells in the epicardium would migrate and differentiate into noncardiomyocytes in myocardium and affect the integrity of ventricular wall,but the underlying mechanism has not been well *** have found that myocardium geranylgeranyl diphosphate synthase(Ggpps),a metabolic enzyme for cholesterol biosynthesis,is critical for cardiac cytoarchitecture remodelling during heart ***,we further reveal that epicardial Ggpps could also regulate ventricular wall architecture ***-specific deletion of Ggpps before embryonic day 10.5(E10.5)is embryonic lethal,whereas after E13.5 is survival but with defects in the epicardium and ventricular wall *** deficiency in the epicardium enhances the proliferation of epicardial cells and disrupts cell‒cell contact,which makes epicardial cells easier to invade into ventricular ***,the fibroblast proliferation and coronary formation in myocardium were found enhanced that might disturb the coronary vasculature remodelling and ventricular wall *** processes might be associated with the activation of YAP signalling,whose nuclear distribution is blocked by Ggpps *** conclusion,our findings reveal a potential link between the cholesterol metabolism and heart epicardium and myocardium development in mammals,which might provide a new view of the cause for congenital heart diseases and potential therapeutic target in pathological cardiac conditions.

关键词： geranylgeranylation Ggpps epicardial cells cell connection myocardium infarction

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Protective effects of hypothermia therapy in ischemia ypoxia-induced cardiomyocyte cell death model:the role of autophagy

Protective effects of hypothermia therapy in ischemia ypoxia...

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第八届海峡两岸心血管科学研讨会

作者：邱碧莹许尧钦张菁萍陈佳莹许传智黄戊田许淑芬张明温郑伯智 Department of Chinese Medicine Chi Mei Medical Center Department of Biotechnology Southern Taiwan University Department of Surgery Chi Mei Medical Center Department of Recreation and Health-Care Management Chia-Nan University of Pharmacy and Science Department of Nursing Shu-Zen College of Medicine and Management Department of Electrical Engineering Southern Taiwan University

Objective Therapeutic hypothermia has been associated as a potential treatment for a number of medical conditions including head injury and cerebral vascular *** the past decade,there have been numerous studies focusing upon the resuscitation following cardiac *** addition,the mechanism of therapeutic hypothermia protection is not completely ***,this cardiomyocyte ischemia reperfusion (I/R) model does demonstrate significant anti - apoptosis and anti - autophage - mediated cardioprotective *** we hypothesized that therapeutic hypothermia would be significantly protected in this model of I/R when induced at start - ischemia or endischemia and maintained into *** H9c2 cells are divided into four groups:Control,Ischemia Reperfusion(I/R),Cooling at Reperfusion(PostTreat) and Cooling at Ischemia(PreTreat).H9c2 cardiomyocytes simulated ischemia/hypoxia by incubation serum and glucose deprived medium and transferred into 0.2%O hypoxia chamber,and then reperfusion replaced into 21%*** H9c2 cells apoptosis was evidenced by flow cytometry -,DNA fragmentation -,and caspase 3 activation - increased apoptotic cells(Annexin -V positive and propidium iodide negative).The H9c2 cells autophagy was evidenced by double immunofluresence stain for lysosome activity,western blot for LC3II protein *** The cell viability was serum deprivation - hypoxia reperfusion reduced significantly and time *** viability loss in the hypoxic serum - starved H9c2 cells was due to apoptosis and *** the 24 - hour I/R injury,the DNA strand breaks and fragmentation occurred in the I/R group,whereas coincidently,the caspase -3,lysosome activity,and LC3II were ***, the percentage of apoptotic cells(flow cytometryanalyzed annexin - V positive and PI negative) significantly increased in I/R *** temperature,especially in PreTreat group,significantly reduced the simulated ischemia - induced cell

关键词： hypothermia autophagy myocardium infarction cardiomyocyte ischemia-reperfusion

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凝集素样氧化低密度脂蛋白受体清除调节系统和局部炎症反应以减弱急性心肌缺血诱导的肾损伤（英文）

凝集素样氧化低密度脂蛋白受体清除调节系统和局部炎症反应以减弱...

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《中华急诊医学杂志》第十一届组稿会暨第四届急诊医学青年论坛

作者：吕菁君魏捷 Wang Xianwei Jawahar L.Mehta 武汉大学人民医院急诊科 Central Arkansas Veterans Healthcare System University of Arkansas for Medical Sciences Departments of Internal Medicine and Pathology Cardiovascular DivisionUniversity of Arkansas for Medical Sciences

ObjectiveTo It is assumed,but never proven,that acute myocardial infarction affects renal *** tested this phenomenon in mice subjected to left coronary artery(LCA)***,we tested the hypothesis that LOX-1 abrogation may inhibit systemic inflammation,collagen accumulation and attenuate renal dysfunction following LCA *** Wild-type(WT)and LOX-1 *** were subjected to permanent LCA ligation resulting in extensive myocardial *** function was analyzed by echocardiography on Day 3 and on Day 21 *** function and morphology were assessed at the same time *** pro-inflammatory signals and markers of fibrosis were measured in the serum and *** after LCA ligation,there was a marked in rise in proinflammatory cytokines and MDA levels in circulation in the WT *** Day 3,renal function assessment showed a marked decline in association with swelling of gomeruli and tubules and mild fibrosis(P<0.05 *** LCA ligation).There was a significant increase in the expression LOX-1,IL-1βand VCAM-1,TBARS levels,and markers of fibrosis(collagenⅣand procollagen-Ⅰ)in the *** Day 21,renal function showed some recovery,but there was extensive fibrosis in the kidneys accompanied with worse LV ***-1 KO mice subjected to total LCA ligation showed much less increase in systemic and renal pro-inflammatory cytokines and MDA levels,and much less structural alterations and functional decline than the WT mice(all P<0.05).Cardiac function and survival rate were better in the LOX-1 KO mice than in the WT mice(P<0.05).ConclusionsWe demonstrate for the first time that severe myocardial ischemia results in renal dysfunction and histologic abnormalities reminiscent of acute renal ***-1 deletion by reducing pro-inflammatory and pro-oxidant signals results in significantly less renal abnormality and *** study suggests that LOX-1 is a key modulator among the multiple mechanisms underlying

关键词： LOX-1 inflammation myocardium infarction renal function

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