title: Angiotensin-Converting Enzyme 2 Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysms in Mice.
abstract: Recent studies have demonstrated that angiotensin-converting enzyme 2 (ACE2) plays an important role in the pathogenesis of abdominal aortic aneurysms (AAAs). However, few studies have reported the direct effect of ACE2 overexpression on the aneurysm. This study hypothesized that the overexpression of ACE2 may prevent the pathogenesis of aneurysms by decreasing RAS activation. Thirty-nine mice were randomly assigned to three groups (n= 13 in each group): the Ad.ACE2 group, theAd.EGFPgroup, and a control group. After 8 weeks of treatment, abdominal aortas with AAAs were obtained for hematoxylin and eosin staining, Verhoeff Van Gieson staining, immunohistochemistry, and Western blotting. The incidence and severity of AAAs, macrophage infiltration, and MMP protein expression were all recorded. The results showed that ACE2 gene transfer significantly decreased the occurrence of AAAs and inhibited AAA formation inApoE-/-mice by inhibiting the inflammatory response and MMP activation, and the mechanisms may involve decreased ERK and Ang II-nuclear factor kappa B signaling pathways.
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, P.R. China.|The Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Shandong, P.R. China.|Department of Physiopathology, Fenyang College Shanxi Medical University, Fenyang, P.R. China.
authors.forename: QingQing
authors.initials: Q
authors.lastname: Hao
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
authors.forename: XueFei
authors.initials: X
authors.lastname: Dong
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, P.R. China.|The Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Shandong, P.R. China.
authors.forename: Xu
authors.initials: X
authors.lastname: Chen
authors.affiliation: The Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Shandong, P.R. China.
authors.forename: Feng
authors.initials: F
authors.lastname: Yan
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, P.R. China.|The Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Shandong, P.R. China.
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
authors.forename: HaiShui
authors.initials: H
authors.lastname: Shi
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, P.R. China.|The Key Laboratory of Cardiovascular Remodeling and Function Research, Shandong University, Shandong, P.R. China.
authors.forename: Bo
authors.initials: B
authors.lastname: Dong
mesh_terms: D000256:Adenoviridae / Q000235:genetics / Q000378:metabolism; D000804:Angiotensin II / Q000008:administration & dosage*; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D001012:Aorta, Abdominal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D017544:Aortic Aneurysm, Abdominal / Q000139:chemically induced / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D015153:Blotting, Western; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D005822:Genetic Vectors / Q000737:chemistry / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D053509:Matrix Metalloproteinase 13 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics* / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics* / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics* / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D001057:Apolipoproteins E; D016328:NF-kappa B; C485184:enhanced green fluorescent protein; D000804:Angiotensin II; D049452:Green Fluorescent Proteins; C535148:Mapk1 protein, mouse; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D007703:Peptidyl-Dipeptidase A; C000705307:ACE2 protein, human; C000705328:Ace2 protein, mouse; D000085962:Angiotensin-Converting Enzyme 2; D053509:Matrix Metalloproteinase 13; C507081:Mmp13 protein, mouse
keywords: ACE2; MMP; aneurysm; inflammation