Open AccessMiR‐195 promotes abdominal aortic aneurysm media remodeling by targeting Smad3
Author(s) -
Liang Bing,
Che Jianbo,
Zhao Hui,
Zhang Zhi,
Shi Gongning
Publication year - 2017
Publication title -
cardiovascular therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 46
eISSN - 1755-5922
pISSN - 1755-5914
DOI - 10.1111/1755-5922.12286
Subject(s) - osteopontin , medicine , vascular smooth muscle , apoptosis , abdominal aortic aneurysm , western blot , cancer research , pathogenesis , flow cytometry , transfection , microrna , cell growth , pathology , microbiology and biotechnology , immunology , cell culture , biology , smooth muscle , aneurysm , gene , biochemistry , surgery , genetics
Summary Introduction MiR‐195 has been implicated in the development of abdominal aortic aneurysms ( AAA ). However, the underlying mechanisms have not been fully addressed. Aim To explore the roles of miR‐195 in regulating the proliferation and apoptosis of vascular smooth muscle cells ( VSMC s), as well as its molecular basis in vitro . Methods qRT ‐ PCR was used to determine the expression levels of miR‐195 and Smad3 in aortic media specimens or VSMC s. Western blot was performed to detect the protein levels of Smad3, osteopontin ( OPN ), and collagen III in aortic media specimens and VSMC s. Luciferase reporter assay was applied to confirm the target of miR‐195 in VSMC s. Proliferation and apoptosis of VSMC s were measured by MTT and flow cytometry, respectively. Results In comparison with the normal controls, the levels of miR‐195, OPN , and collagen III were significantly increased in AAA tissue. Smad3 was validated to be a direct target of miR‐195. miR‐195 inhibited proliferation and induced apoptosis of VSMC s, which was abated by Smad3 overexpression. Expression of OPN and collagen III was improved in VSMC s after transfection with miR‐195 mimics, while up‐regulation of Smad3 reversed this effect. Conclusion MiR‐195 promotes media remodeling by targeting Smad3 in AAA progression. This study suggests that miR‐195 contributes to the pathogenesis of AAA and reveals a new targeted therapy strategy for AAA patients.