Myeloid HIF-1 attenuates the progression of renal fibrosis in murine obstructive nephropathy

Yu Tateishi, Mayuko Osada-Oka, Masako Tanaka, Masayuki Shiota, Yasukatsu Izumi, Eiji Ishimura, Koka Motoyama, Masaaki Inaba, Katsuyuki Miura

研究成果: Article査読

11 被引用数 (Scopus)

抄録

Hypoxia-inducible factors (HIFs) play an important role in the pathogenesis of renal fibrosis. Although the role of macrophage infiltration in the progression of renal fibrosis is well known, the role of macrophage HIF-1 remains to be revealed. To address this question, myeloid specific conditional HIF-1 knock out mice were subjected to unilateral ureteral obstruction (UUO). Renal interstitial deposition of collagen III and mRNA expressions of collagen I and collagen III were markedly increased at 7 days after UUO and myeloid HIF-1 depletion significantly accelerated these increases. Immunohistochemistry and flow cytometric analysis revealed that renal infiltrating macrophages were increased with duration of UUO but myeloid HIF-1 depletion did not affect these changes. Myeloid HIF-1 depletion did not affect M1 and M2 macrophage phenotype polarization in obstructed kidneys. Renal connective tissue growth factor (CTGF) expression was markedly increased and myeloid HIF-1 depletion further enhanced this increase. Immunomagnetic separation of renal cells revealed that renal CTGF was expressed predominantly in renal cells other than macrophages. It is suggested that myeloid HIF-1 attenuates the progression of renal fibrosis in murine obstructive kidney. Alteration of CTGF expression in renal cells other than macrophages is one of possible mechanisms by which myeloid HIF-1 protected renal fibrosis.

本文言語English
ページ(範囲)181-189
ページ数9
ジャーナルJournal of Pharmacological Sciences
127
2
DOI
出版ステータスPublished - 2015
外部発表はい

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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