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Study On The Mechanism Of ACE2 Inhibiting Cell Proliferation In Pulmonary Arterial Hypertension

Posted on:2021-12-15Degree:MasterType:Thesis
Country:ChinaCandidate:R WangFull Text:PDF
GTID:2514306473965849Subject:Anesthesia
Abstract/Summary:PDF Full Text Request
Objective FAK is an important therapeutic target for PAH,but the upstream mediator remains unknown.This study aimed to investigate whether ACE2 could regulate FAK and alleviate PAH.Method First,the right ventricular pressure,body weight,right ventricular hypertrophy index,and HE staining of each group were measured to determine whether the modeling was successful.We initially observed the changes in serum levels of FAK to assess the correlation between ACE2 and FAK.Then the expression of related proteins in the pathway was determined by western blot(WB),q PCR and immunohistochemistry.Finally,the apoptosis of PASMCs around pulmonary arterioles was observed by tunel staining.Results(1)ACE2 alleviates PAH morphology.(2)ACE2 can inhibit FAK content in serum.(3)WB and q PCR results showed that ACE2 can inhibit the expression of FAK and pathway-related proteins,but promote the expression of caspase-3.(4)ACE2 can inhibit the expression of FAK around the pulmonary arterioles and promote PASMCs apoptosis.Conclusions The activation of ACE2 inhibits the expression of FAK and pathway-related proteins,and promotes the expression of caspase-3,achieving the purpose of inhibiting cell proliferation in PAH.
Keywords/Search Tags:Pulmonary hypertension, Focal adhesion kinase, Angiotensin converting enzyme 2, Apoptosis
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