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Signal transducer and activator of transcription 3 involvement in the development of renal interstitial fibrosis after unilateral ureteral obstruction
Author(s) -
KURATSUNE MASATOSHI,
MASAKI TAKAO,
HIRAI TAKAYUKI,
KIRIBAYASHI KEI,
YOKOYAMA YUKIO,
ARAKAWA TETSUJI,
YORIOKA NORIAKI,
KOHNO NOBUOKI
Publication year - 2007
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2007.00881.x
Subject(s) - stat3 , medicine , myofibroblast , immunostaining , stat protein , fibrosis , blot , pathology , western blot , in vivo , kidney , immunohistochemistry , cancer research , phosphorylation , biology , microbiology and biotechnology , biochemistry , gene
SUMMARY: Background: In vitro studies suggest that the signal transducer and activator of transcription (STAT) plays a critical role in renal fibrosis. However, the process of STAT activation in vivo remains unclear. This study in rats aimed to localize STAT3 activation within the kidney and examine the in vivo relationship between STAT3 activation and renal fibrosis. Methods: Unilateral ureteral obstruction (UUO) was induced in the rats and the kidneys examined 3 or 7 days after obstruction. Activation of STAT3 in western blot and immunohistochemical analyses was identified by the phosphorylated form of STAT3 (pSTAT3). Results: Myofibroblasts were identified by α‐smooth muscle actin expression and were upregulated in obstructed kidneys. pSTAT3 was localized mainly in tubular epithelial cells of collecting ducts in normal and obstructed kidneys and interstitial cells in obstructed kidneys. After UUO, western blotting showed a fourfold increase in pSTAT3, with a peak at day 7. Immunostaining showed a sixfold increase in pSTAT3 at day 7 in tubular epithelial cells and a 2500‐fold increase at day 7 in interstitial cells. Conclusion: STAT3 was activated in rat tubular epithelial cells and myofibroblasts after UUO, suggesting that STAT3 may contribute to the progression of interstitial fibrosis.