| First Author | Neelisetty S | Year | 2015 |
| Journal | Kidney Int | Volume | 88 |
| Issue | 3 | Pages | 503-14 |
| PubMed ID | 25760325 | Mgi Jnum | J:323120 |
| Mgi Id | MGI:7261416 | Doi | 10.1038/ki.2015.51 |
| Citation | Neelisetty S, et al. (2015) Renal fibrosis is not reduced by blocking transforming growth factor-beta signaling in matrix-producing interstitial cells. Kidney Int 88(3):503-14 |
| abstractText | Transforming growth factor-beta (TGF-beta) strongly promotes renal tubulointerstitial fibrosis, but the cellular target that mediates its profibrotic actions has not been clearly identified. While in vitro data suggest that TGF-beta-induced matrix production is mediated by renal fibroblasts, the role of these cells in TGF-beta-dependent tubulointerstitial fibrosis following renal injury is not well defined. To address this, we deleted the TGF-beta type II receptor in matrix-producing interstitial cells using two different inducible Cre models: COL1A2-Cre with a mesenchymal enhancer element and tenascin-Cre that targets medullary interstitial cells, and either the mouse unilateral ureteral obstruction or the aristolochic acid renal injury model. Renal interstitial cells lacking the TGF-beta receptor had significantly impaired collagen I production, but, unexpectedly, overall tissue fibrosis was unchanged in the conditional knockouts after renal injury. Thus, abrogating TGF-beta signaling in matrix-producing interstitial cells is not sufficient to reduce fibrosis after renal injury. |
