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MiR-195 promotes abdominal aortic aneurysm media remodeling by targeting Smad3
Bing Liang1, Jianbo Che1, Hui Zhao1
1Department of Cardiothoracic Surgery, Huaihe Hospital of Henan University, Kaifeng, China.
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 (VSMCs), 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 VSMCs. Western blot was performed to detect the protein levels of Smad3, osteopontin (OPN), and collagen III in aortic media specimens and VSMCs. Luciferase reporter assay was applied to confirm the target of miR-195 in VSMCs. Proliferation and apoptosis of VSMCs 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 VSMCs, which was abated by Smad3 overexpression. Expression of OPN and collagen III was improved in VSMCs 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.
Insights
MicroRNA-195 (miR-195) promotes abdominal aortic aneurysm (AAA) progression by targeting Smad3. This finding reveals miR-195 as a potential therapeutic target for AAA.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Atherosclerosis Research
Background:
- Abdominal aortic aneurysm (AAA) pathogenesis involves complex molecular mechanisms.
- MicroRNA-195 (miR-195) is implicated in AAA development, but its precise role remains unclear.
Purpose of the Study:
- To investigate the function of miR-195 in vascular smooth muscle cell (VSMC) proliferation and apoptosis.
- To elucidate the molecular targets and pathways regulated by miR-195 in vitro.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for miR-195 and Smad3 expression.
- Western blot analysis for Smad3, osteopontin (OPN), and collagen III protein levels.
- Luciferase reporter assays, MTT assays, and flow cytometry to assess miR-195 targets and VSMC functions.
Main Results:
- miR-195, OPN, and collagen III levels were elevated in AAA tissues compared to controls.
- Smad3 was confirmed as a direct target of miR-195.
- miR-195 inhibited VSMC proliferation and induced apoptosis, effects reversed by Smad3 overexpression; OPN and collagen III expression changes were similarly modulated by miR-195 and Smad3.
Conclusions:
- MiR-195 promotes vascular media remodeling in AAA by targeting Smad3.
- This study identifies miR-195 as a key contributor to AAA pathogenesis.
- miR-195 presents a novel therapeutic target for managing AAA.
