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Publication : UT-A1/A3 knockout mice show reduced fibrosis following unilateral ureteral obstruction.

First Author  Rianto F Year  2020
Journal  Am J Physiol Renal Physiol Volume  318
Issue  5 Pages  F1160-F1166
PubMed ID  32174141 Mgi Jnum  J:294348
Mgi Id  MGI:6451248 Doi  10.1152/ajprenal.00008.2020
Citation  Rianto F, et al. (2020) UT-A1/A3 knockout mice show reduced fibrosis following unilateral ureteral obstruction. Am J Physiol Renal Physiol 318(5):F1160-F1166
abstractText  Renal fibrosis is a major contributor to the development and progression of chronic kidney disease. A low-protein diet can reduce the progression of chronic kidney disease and reduce the development of renal fibrosis, although the mechanism is not well understood. Urea reabsorption into the inner medulla is regulated by inner medullary urea transporter (UT)-A1 and UT-A3. Inhibition or knockout of UT-A1/A3 will reduce interstitial urea accumulation, which may be beneficial in reducing renal fibrosis. To test this hypothesis, the effect of unilateral ureteral obstruction (UUO) was compared in wild-type (WT) and UT-A1/A3 knockout mice. UUO causes increased extracellular matrix associated with increases in transforming growth factor-beta, vimentin, and alpha-smooth muscle actin (alpha-SMA). In WT mice, UUO increased the abundance of three markers of fibrosis: transforming growth factor-beta, vimentin, and alpha-SMA. In contrast, in UT-A1/A3 knockout mice, the increase following UUO was significantly reduced. Consistent with the Western blot results, immunohistochemical staining showed that the levels of vimentin and alpha-SMA were increased in WT mice with UUO and that the increase was reduced in UT-A1/A3 knockout mice with UUO. Masson's trichrome staining showed increased collagen in WT mice with UUO, which was reduced in UT-A1/A3 knockout mice with UUO. We conclude that reduced UT activity reduces the severity of renal fibrosis following UUO.
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