| First Author | Hung CF | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 5 | Pages | e0197937 |
| PubMed ID | 29813125 | Mgi Jnum | J:262385 |
| Mgi Id | MGI:6160371 | Doi | 10.1371/journal.pone.0197937 |
| Citation | Hung CF, et al. (2018) Role of integrin alpha8 in murine model of lung fibrosis. PLoS One 13(5):e0197937 |
| abstractText | BACKGROUND: Integrin alpha8 (ITGA8) heterodimerizes with integrin beta1 and is highly expressed in stromal cells of the lung. Platelet-derived growth factor receptor beta (PDGFRbeta+) cells constitute a major population of contractile myofibroblasts in the lung following bleomycin-induced fibrosis. Integrin alpha8beta1 is upregulated in fibrotic foci in bleomycin-induced lung injury. However, the functional role of ITGA8 in fibrogenesis has not been characterized. In this study, we examined whether genetic deletion of ITGA8 from PDGFRbeta+ cells in the lung altered fibrosis. METHODS: Pdgfrb-Cre/+;Itga8flox/- or Pdgfrb-Cre/+;Itga8flox/flox (Cre+) and control mice (Cre-) were used for in vitro and in vivo studies. Primary cultures of PDGFRbeta+ cells were exposed to TGFbeta, followed by RNA isolation for qPCR. For in vivo studies, Cre+ and Cre- mice were characterized at baseline and after bleomycin-induced fibrosis. RESULTS: PDGFRbeta-selected cells from Cre+ animals showed higher levels of Col1a1 expression after treatment with TGFbeta. However, Cre- and Cre+ animals showed no significant difference in measures of acute lung injury or fibrosis following bleomycin challenge. CONCLUSION: While ITGA8 deletion in lung PDGFRbeta+ stromal cells showed evidence of greater Col1a1 mRNA expression after TGFbeta treatment in vitro, no functional difference was detected in vivo. |
