The Expression Of AT1Receptor Protein In Vascular Smooth Muscle Cells After ACE2Sirna Interference

Objective: To investigate the effect of angiotensin II type1receptor（AT1R）expression and the level of extracelluar signal-regulated kinase (ERK1/2) and signaltransducer and activator of transcription3（STAT3）phosphorylation with the lessexpression of ACE2protein after ACE2si-RNA interference in vascular smoothmuscle cells (VSMCs).Methods:（1）In corresponding group the SD rat vascular smooth muscle cells(VSMCs) was transfected by pm-ACE2and si-ACE2through lipofectamine2000andused tissue culture method explant;（2） The VSMCs were divided into10groups:control group; lentiviral-GFP group （GFP）;lipofectamine2000group;lentiviral-ACE2group;si-ACE2group;AngII group;AngII+lentiviral-ACE2group;AngII+lentiviral-ACE2+si-ACE2group;AngII+siACE-2group;scrambledsiRNA group.（3）ACE2、AT1R protein expression,P-ERK1/2and P-STAT3proteinphosphorylation level were detected with western blot after the si-ACE2were addedinto certain groups.Results:Western-Blot showed that the amount of ACE2protein in si-ACE2group andAngII group was less than that in the control group、lipofectamine2000group andGFP group(P<0.05);In contrast, the AT1R protein expression and the level ofP-ERK1/2、P-STAT3phosphorylation in si-ACE2group and AngII group were muchhigher than those in the control group、 lipofectamine2000group and GFPgroup(P<0.05);Compared to AngII group the AngII+si-ACE2group ACE2protein expression was also significantly less (P<0.05),and the AT1R protein expression andthe level of P-ERK1/2、P-STAT3phosphorylation were much higher(P<0.05).Conclusion:The expression of ACE2gene in VSMCs could be significantly inhibitedby si-RNA and AngII.Besides,si-ACE2and AngII can synergistically inhibit theexpression of ACE2protein.With the less express of ACE2gene can upregulate AT1receptor expression and signal pathway of P-ERK1/2and P-STAT3phosphorylationlevel.