ArticleBioscience reports2020
Physiological cyclic stretch up-regulates angiotensin-converting enzyme 2 expression to reduce proliferation and migration of vascular smooth muscle cells.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Distinct molecular profiles in human aortic smooth muscle cells under cyclic stretch and hydrostatic pressure.The journal of physiological sciences : JPS · 2026Article
- Cyclic stretch inhibits cell invasion in 3D scaffolds.bioRxiv : the preprint server for biology · 2026Article
- Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026Review
- ACE2 Inhibits Dermal Regeneration Through Ang II in Tissue Expansion.Journal of cosmetic dermatology · 2025Article
- Gene expression modulation in human aortic smooth muscle cells under induced physiological mechanical stretch.Scientific reports · 2024Article
- Towards a more objective and high-throughput spheroid invasion assay quantification method.Scientific reports · 2024Article
- Towards a More Objective and High-throughput Spheroid Invasion Assay Quantification Method.bioRxiv : the preprint server for biology · 2024Article
- CDK4/6 inhibitor palbociclib promotes SARS-CoV-2 cell entry by down-regulating SKP2 dependent ACE2 degradation.Antiviral research · 2023Article
- N-3 polyunsaturated fatty acids block the trimethylamine-N-oxide- ACE2- TMPRSS2 cascade to inhibit the infection of human endothelial progenitor cells by SARS-CoV-2.The Journal of nutritional biochemistry · 2022Article
- Mechano-inflammatory sensitivity of ACE2: Implications for the regional distribution of SARS-CoV-2 injury in the lung.Respiratory physiology & neurobiology · 2022Article
- Article
- Review
- ACE2/Ang-(1-7)/Mas1 axis and the vascular system: vasoprotection to COVID-19-associated vascular disease.Clinical science (London, England : 1979) · 2021Review
- Vascular Endothelial Dysfunction and Immunothrombosis in the Pathogenesis of Atrial Fibrillation.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin-converting enzyme 2 (ACE2) is considered as an endogenous negative regulator of renin-angiotensin system (RAS), exerting multiple cardiovascular protective roles. Whether mechanical stretch modulates ACE2 expression remains unknown. The present study aimed at investigating whether ACE2 is involved in physiological stretch (10% elongation, 1 Hz) mediated cellular functions and the underlying mechanism. Cultured human aortic smooth muscle cells (HASMCs) were exposed to 10% stretch for indicated time, and real-time PCR and Western blot analysis showed 10% stretch increased ACE2 expression and activity significantly compared with static conditions and increased Ang-(1-7) level, but decreased Ang II level; Brdu incorporation assay and Scratch test showed that ACE2 was involved in the inhibition of HASMCs proliferation and migration by 10% stretch; the Dual-Luciferase Reporter Assay demonstrated that 10% increased ACE2 promoter activity, but had no effect on ACE2 mRNA stability; kinase inhibition study and Electrophoretic mobility shift assay (EMSA) showed that JNK1/2 and PKCβII pathway, as well as their downstream transcription factors, AP-1 and NF-κB, were involved in 10% stretch induced ACE2 expression. In conclusion, our study indicates ACE2 is a mechanosensitive gene, and may represent a potential therapeutic target for mechanical forces related vascular diseases.
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