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TRPV4 contributes to renal injury induced by angiotensin II in mice
Author(s) -
Wang Youping,
Zhu Minjun,
Cui Lin,
Liu Weihong,
Wang Xiaoxiao,
Shen Si,
Xu Hui
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb731
Subject(s) - medicine , endocrinology , glomerulosclerosis , angiotensin ii , sirius red , renal injury , chemistry , blood pressure , kidney , fibrosis , proteinuria
To determine whether deletion of TRPV4 attenuates angiotensin II (Ang II)‐induced renal injury, Ang II was infused systemically into wild type (WT) and TRPV4‐null mutant (TRPV4 ‐/‐ ) mice for 4 weeks. Systolic blood pressure increased in Ang II‐treated WT or TRPV4 ‐/‐ mice with the similar degree (P>0.05). Ang II treatment increased urinary excretion of albumin and 8‐isoprostane, and decreased creatinine clearance in both WT and TRPV4 ‐/‐ mice with a greater magnitude in the former strain (P<0.05). Periodic acid‐Schiff and Masson's trichrome staining showed that kidneys of Ang II‐treated WT mice exhibited more severe glomerulosclerosis and tubulointerstitial injury compared with Ang II‐treated TRPV4 ‐/‐ mice (P<0.05). Hydroxyproline assay and F4/80‐staining showed that renal collagen levels and monocyte/macrophage infiltration were greater in Ang II‐treated WT mice compared with TRPV4 ‐/‐ mice (P<0.05). Thus, our data show that deletion of TRPV4 alleviates renal injury in the absence of alteration in blood pressure in Ang II‐hypertensive mice, indicating that TRPV4 could serve as a novel target for treating renal injury associated with hypertension. [This work was supported by grants from the National Natural Science Foundation of China (No.81170243) and Henan Provincial Science and Technology Innovative Program for Outstanding Scholarship (No. 124200510007)].