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Updated: Jun 12, 2025

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
Published on: June 11, 2017
S1PR2 Mediates Smooth Muscle Cell Proliferation and Endothelial Cell Permeability via Akt/mTOR and RhoA/ROCK1 in
Jie Ouyang1,2, Haijiao Long2, Shuhua Chen3
1Health Management Center, the Third Xiangya Hospital of Central South University, Changsha, China.
Sphingosine 1-phosphate receptor 2 (S1PR2) has a dual role in atherosclerosis. Targeting specific cell types involving S1PR2 may offer promise for treating this complex vascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cell Signaling
Background:
- Atherosclerosis involves endothelial dysfunction and smooth muscle cell proliferation.
- Sphingosine 1-phosphate receptors (S1PRs) are implicated in atherosclerosis pathogenesis.
- The precise role of S1PRs in atherosclerosis remains unclear.
Purpose of the Study:
- To elucidate the dual role of S1PR2 in vascular cells during atherosclerosis.
- To investigate the signaling pathways regulated by S1PR2 in endothelial and smooth muscle cells.
- To evaluate the therapeutic potential of targeting S1PR2 in an atherosclerosis mouse model.
Main Methods:
- Utilized oxidized-low-density lipoprotein (ox-LDL) to treat vascular cells.
- Investigated S1PR2 expression and downstream signaling pathways (Akt/mTOR, RhoA/ROCK1).
- Employed an apolipoprotein E-deficient mouse model with S1PR2 agonist and antagonist treatments.
Main Results:
- In smooth muscle cells, decreased S1PR2 upregulated PCNA via Akt/mTOR, promoting proliferation.
- In endothelial cells, elevated S1PR2 reduced VE-cadherin via RhoA/ROCK1, increasing permeability.
- S1PR2 modulation showed opposing effects in vivo, limiting plaque reduction efficacy.
Conclusions:
- S1PR2 exhibits opposing functions in endothelial and smooth muscle cells relevant to atherosclerosis.
- Targeting S1PR2 specifically within cell types may be a promising therapeutic strategy.
- S1PR2 presents a potential target for atherosclerosis prevention and treatment.
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