| First Author | Yukawa K | Year | 2005 |
| Journal | Int J Mol Med | Volume | 15 |
| Issue | 2 | Pages | 225-30 |
| PubMed ID | 15647835 | Mgi Jnum | J:100543 |
| Mgi Id | MGI:3588820 | Citation | Yukawa K, et al. (2005) STAT6 deficiency inhibits tubulointerstitial fibrosis in obstructive nephropathy. Int J Mol Med 15(2):225-30 |
| abstractText | To elucidate the contribution of signal transducer and activator of transcription (STAT) 6 to the pathophysiology of chronic renal injury, STAT6-/- mice were subjected to unilateral ureteral ligation together with wild-type control mice. STAT6-/- kidneys had more apoptotic cells and a greater influx of F4/80-positive cells than wild-type kidneys following ureteral obstruction. There was a much larger alpha-smooth muscle actin-positive area in STAT6-/- kidneys than in wild-type kidneys after ureteral ligation. However, renal fibrosis, as quantified by Masson-Trichrome staining, was not significantly exaggerated in STAT6-/- kidneys compared with wild-type kidneys. The accumulation of collagen I was significantly less in STAT6-/- kidneys than in wild-type kidneys. These observations indicate that the STAT6 signal transduction pathway exerts a protective role on renal cell apoptosis in chronic obstructive uropathy. Our findings also suggest that the STAT6 pathway may have a promotive effect on renal fibrosis by activating collagen synthesis following ureteral obstruction. |
