The Mechanism of Tight Junction Protein 5 in Perioperative Stress-induced Heart Disease
ZHOU Xinzhi
ZHANG Song
LI Yinyu
WEI Xiaodong
Abstract：Objective:To explore the mechanism of tight junction protein 5(Claudin-5)in perioperative stress-induced heart disease.Methods:AC16 human cardiac muscle cell lines were cultured and divided into sham group and ischaemia/reperfusion injury(I/R)group.The Claudin-5 infected with silent RNA knockdown and adenovirus was divided into normal group(N group),hypoxia/reoxygenation(H/R)group,H/R+Claudin-5 specific small interfering RNA(siRNA)group and H/R+Claudin-5 overexpression adenovirus(Adv)group.Claudin-5,cytochrome C release and caspase 3 in mouse cardiac tissues and neonatal mouse cardiomyocytes(NRCM)were detected by Western Blot.Cardiac sections of Wild-type and Claudin-5 Adv mice were stained with 2,3,5-triphenyltetrazolium chloride(TTC).The cardiac functions of Wild-type and Claudin-5 Adv mice were quantitatively analyzed by echocardiographic imaging.Results:The expression of Claudin-5 in the heart was down-regulated after myocardial I/R injury in vitro and in vivo.Overexpression of Claudin-5 significantly inhibited the apoptotic process,while reduced cytochrome C release and Caspase 3 cleavage.TTC staining indicated that overexpression of Claudin-5 showed an anti-apoptotic effect.Compared with the sham group,left ventricular shortening score(LVFS)improved in myocardial I/R injury after Claudin-5 overexpression.Conclusion:Claudin-5 showed an anti-apoptotic effect on the myocardium and could counteract myocardial I/R injury,suggesting that it could be used as a therapeutic target for perioperative stress-induced heart disease.
Keywords：perioperative stress-induced heart diseasetight junction protein 5cytochrome CCaspase 3miceexperimental study
Publication Date：2025-09-25
Online Publishing Date：2025-10-14(First online date of this platform, not the publication date of the document)
Pages：6( 2776-2781 )