STAT1 activation regulates proliferation and differentiation of renal progenitors.

Cellular Signalling
Honghe WangAlan O Perantoni

Abstract

We have shown previously that activation of STAT1 contributes to the pathogenesis of Wilms tumor. This neoplasm caricatures metanephric development and is believed to originate from embryonic renal mesenchymal progenitors that lose their ability to undergo mesenchymal-epithelial transition (MET). Therefore, we hypothesized that STAT1 is also activated and functional during metanephric development. Here we have demonstrated that both STAT1 and STAT3 are activated during normal development of the embryonic kidney. Furthermore, activation of STAT1 stimulated the proliferation of metanephric mesenchymal cells, but it prevented MET and tubulogenesis induced by leukemia inhibitory factor, which preferentially activates STAT3. Consistent with its negative regulation of metanephric mesenchymal differentiation, inhibition of STAT1 activation with protein kinase CK2 inhibitor TBB or RNAi-mediated knockdown of STAT1 promoted differentiation of metanephric progenitors and abolished the effect of cytokine-induced STAT1 activation in these cells. Additionally, a cell-permeable peptide that inhibits STAT1-mediated transactivation by targeting the STAT1 N-domain also blocked cytokine-induced STAT1-dependent proliferation in metanephric progeni...Continue Reading

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Citations

Jul 19, 2012·Asian Pacific Journal of Tropical Medicine·Zeng LiangMing Li
Nov 29, 2011·Cellular Signalling·You-Na JangEun Joo Baik
Jul 16, 2014·Biochimica Et Biophysica Acta·Fang TianYili Yang
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Jul 1, 2012·JAK-STAT·Sarah G BaileyPaul A Townsend
May 10, 2017·International Reviews of Immunology·Marla Karine AmaranteMaria Angelica Ehara Watanabe
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Jan 10, 2020·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Nihal KaplanRobert M Lavker
Oct 13, 2020·Cancer Biology & Therapy·Fangran LiuGuoxiong Xu
May 23, 2012·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Nikolai N KhodarevRalph R Weichselbaum

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