| First Author | Jung IH | Year | 2024 |
| Journal | Heliyon | Volume | 10 |
| Issue | 4 | Pages | e25760 |
| PubMed ID | 38370227 | Mgi Jnum | J:389043 |
| Mgi Id | MGI:7856037 | Doi | 10.1016/j.heliyon.2024.e25760 |
| Citation | Jung IH, et al. (2024) Integrin alpha9beta1 deficiency does not impact the development of atherosclerosis in mice. Heliyon 10(4):e25760 |
| abstractText | Sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1 (SVEP1) is an extracellular matrix protein that causally promotes cardiovascular disease in humans and mice. However, the receptor mediating the effect of SVEP1 on the development of disease remains unclear. We previously demonstrated that depleting either vascular smooth muscle cell (VSMC)- or myeloid cell-derived integrin alpha9beta1, the first receptor that was identified to interact with SVEP1, did not phenocopy the disease-abrogating effect of depleting SVEP1. Due to its wide expression in tissues and cell types, here we extend this line of investigation to definitively determine if integrin alpha9beta1 impacts the development of atherosclerosis. In a mouse model of atherosclerosis, we found that depleting integrin alpha9beta1 in all cells did not alter plaque size or characteristics of plaque complexity when compared to wild type mice. Further, the significant SVEP1-mediated effects on increase in macrophage content and VSMC proliferation within the atherosclerotic plaque were not altered in animals lacking integrin alpha9beta1. Together, these findings strongly suggest that integrin alpha9beta1 is not responsible for mediating the SVEP1-induced promotion of atherosclerosis and support further studies aimed at characterizing other receptors whose interaction with SVEP1 may represent a therapeutically targetable interaction. |
