Sialyltransferase7A Promotes Myocardial Hypertrophy Induced By AngⅡ In Wistar Rat

Objective: Sialylation regulates human embryonic heart development and cardiac function.Studies have shown that sialylation is further enhanced when cardiac hypertrophy occurs.Sialyltransferases are involved in sialylation,the study found that in three rat models of hypertensive myocardial hypertrophy with different genetic backgrounds,when genetic testing was associated with hypertension,myocardial hypertrophy and chromosome distribution,only genes encoding sialyltransferase 7A (Siat7A)persisted expression.But whether Siat7 A has a regulatory effect on the occurrence and development of myocardial hypertrophy has not yet been reported.Therefore,the purpose of this study was to explore the regulatory effects of Siat7 A on blood pressure,cardiac function and myocardial hypertrophy and find a new target for the clinical treatment.Materials and methods: 8-week-old male Wistar rats,were injected in situ into the myocardium with adeno-associated virus carrying sh Siat7 A plasmid or injected into the external jugular vein with adeno-associated virus carrying the over Siat7 A plasmid,simutanously,Angiotensin Ⅱ(AngⅡ)was continuously infused to promote myocardial hypertrophy in rats.Adeno-associated virus infection was detected by bioluminescence imaging technology;blood pressure was measured by blood pressure measuring instrument;heart function and left ventricular hypertrophy were observed by cardiac echocardiograph;the heart weight/body weight(HW/BW)was obtained by weighing the weight of rat and wet heart weight.Hematoxylin(HE)staining was applied to observe myocardial histopathology.The expression of Siat7 A in myocardial tissue was detected by Western blot;the expression of Siat7 A,atrial natriuretic peptide(ANP) and B-type natriuretic peptide(BNP)in tissues were detected by Real-Time PCR.Results: Compared with the saline-injected rat hearts,the adeno-associated virus-injected hearts had obvious green fluorescent protein expression,indicating that the adeno-associated virus successfully infected the heart.Continuous blood pressure monitoring and echocardiography confirmed that the myocardial hypertrophy rat model was successfully constructed.Chronically infusion of AngⅡ obviously elevated the mean arterial pressure(MAP)to a high level.Long-term hypertention significantly reduced the left ventricular end-systolic dimension(LVID-s),increased the left ventricular end-systolic posterior wall thickness(LVPW-s)and Left ventricular ejection fraction(EF%),as well as left ventricular fractional shortening(FS%).Furthermore,cardiomyocyte hypertrophy induced by AngⅡ was shown as myocardial alignment disorder,nucleus enlargement and malformation,increased HW/BW.Meanwhile,the expressions of Siat7 A,ANP and BNP were significantly increased.Knocking down the expression of Siat7 A gene,the decrease in LVID-s and the increase in LVPW-s were significantly inhibited,the increase in EF% and FS% were depressed,and the expressions of ANP and BNP were decreased.Over-expression of Siat7 A gene caused more increase in EF% and FS% and aggravated cardiac dysfunction.In terms of myocardial hypertrophy factors,the expressions of ANP and BNP were further increased.Conclusions: 1.Siat7 A expression was increased in AngⅡ-induced myocardial hypertrophy in rat.2.Knockdown of Sait7 A could significantly inhibit the development of myocardial hypertrophy induced by AngⅡ.3.Overexpression of Sait7 A could promote the development of myocardial hypertrophy induced by AngⅡ.