| First Author | Li Z | Year | 2013 |
| Journal | Am J Pathol | Volume | 182 |
| Issue | 2 | Pages | 325-31 |
| PubMed ID | 23195429 | Mgi Jnum | J:192574 |
| Mgi Id | MGI:5465390 | Doi | 10.1016/j.ajpath.2012.10.022 |
| Citation | Li Z, et al. (2013) Caveolin-1 Deficiency Induces Spontaneous Endothelial-to-Mesenchymal Transition in Murine Pulmonary Endothelial Cells in Vitro. Am J Pathol 182(2):325-31 |
| abstractText | It was previously demonstrated that transforming growth factor beta (TGF-beta) induces endothelial-to-mesenchymal transition (EndoMT) in murine lung endothelial cells (ECs) in vitro. Owing to the important role of caveolin-1 (CAV1) in TGF-beta receptor internalization and TGF-beta signaling, the participation of CAV1 in the induction of EndoMT in murine lung ECs was investigated. Pulmonary ECs were isolated from wild-type and Cav1 knockout mice using immunomagnetic methods with sequential anti-CD31 and anti-CD102 antibody selection followed by in vitro culture and treatment with TGF-beta1. EndoMT was assessed by semiquantitative RT-PCR for Acta2, Col1a1, Snai1, and Snai2; by immunofluorescence for alpha-smooth muscle actin; and by Western blot analysis for alpha-smooth muscle actin, SNAIL1, SNAIL2, and the alpha2 chain of type I collagen. The same studies were performed in Cav1(-/-) pulmonary ECs after restoration of functional CAV1 domains using a cell-permeable CAV1 scaffolding domain peptide. Pulmonary ECs from Cav1 knockout mice displayed high levels of spontaneous Acta2, Col1A, Snai1, and Snai2 expression, which increased after TGF-beta treatment. Spontaneous and TGF-beta1-stimulated EndoMT were abrogated by the restoration of functional CAV1 domains using a cell-permeable peptide. The findings suggest that CAV1 regulation of EndoMT may play a role in the development of fibroproliferative vasculopathies. |
