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  • The loss of Krüppel-like factor 15 in Foxd1+ stromal cells exacerbates kidney fibrosis.

The loss of Krüppel-like factor 15 in Foxd1+ stromal cells exacerbates kidney fibrosis.

Kidney international (2017-06-28)
Xiangchen Gu, Sandeep K Mallipattu, Yiqing Guo, Monica P Revelo, Jesse Pace, Timothy Miller, Xiang Gao, Mukesh K Jain, Agnieszka B Bialkowska, Vincent W Yang, John C He, Changlin Mei
摘要

Large epidemiological studies clearly demonstrate that multiple episodes of acute kidney injury contribute to the development and progression of kidney fibrosis. Although our understanding of kidney fibrosis has improved in the past two decades, we have limited therapeutic strategies to halt its progression. Myofibroblast differentiation and proliferation remain critical to the progression of kidney fibrosis. Although canonical Wnt signaling can trigger the activation of myofibroblasts in the kidney, mediators of Wnt inhibition in the resident progenitor cells are unclear. Recent studies demonstrate that the loss of a Krüppel-like factor 15 (KLF15), a kidney-enriched zinc-finger transcription factor, exacerbates kidney fibrosis in murine models. Here, we tested whether Klf15 mRNA and protein expression are reduced in late stages of fibrosis in mice that underwent unilateral ureteric obstruction, a model of progressive renal fibrosis. Knockdown of Klf15 in Foxd1-expressing cells (Foxd1-Cre Klf15fl/fl) increased extracellular matrix deposition and myofibroblast proliferation as compared to wildtype (Foxd1-Cre Klf15+/+) mice after three and seven days of ureteral obstruction. This was validated in mice receiving angiotensin II treatment for six weeks. In both these murine models, the increase in renal fibrosis was found in Foxd1-Cre Klf15fl/fl mice and accompanied by the activation of Wnt/β-catenin signaling. Furthermore, knockdown of Klf15 in cultured mouse embryonic fibroblasts activated canonical Wnt/β-catenin signaling, increased profibrotic transcripts, and increased proliferation after treatment with a Wnt1 ligand. Conversely, the overexpression of KLF15 inhibited phospho-β-catenin (Ser552) expression in Wnt1-treated cells. Thus, KLF15 has a critical role in attenuating kidney fibrosis by inhibiting the canonical Wnt/β-catenin pathway.

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抗肌动蛋白,α-平滑肌抗体,小鼠单克隆, clone 1A4, purified from hybridoma cell culture
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CN¥1,614.82
250 mg
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1 g
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Sigma-Aldrich
Anti-GAPDH,克隆6C5, clone 6C5, Chemicon®, from mouse
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货号包装规格是否有货价格数量
100 mg
国内现货,预计发货时间 April 07, 2025
详情...
CN¥1,614.82
250 mg
国内现货,预计发货时间 April 07, 2025
详情...
CN¥2,669.26
1 g
请联系客服了解存货情况
CN¥7,772.55
Sigma-Aldrich
抗-KLF15抗体, 1.0 mg/mL, from rabbit
登录查看公司和协议定价
货号包装规格是否有货价格数量
100 mg
国内现货,预计发货时间 April 07, 2025
详情...
CN¥1,614.82
250 mg
国内现货,预计发货时间 April 07, 2025
详情...
CN¥2,669.26
1 g
请联系客服了解存货情况
CN¥7,772.55