Knockout of TRPA1 exacerbates angiotensin II-induced kidney injury.

Knockout of TRPA1 exacerbates angiotensin II-induced kidney injury. Am J Physiol Renal Physiol. 2019 Jul 24;: Authors: Ma S, Zhang Y, He K, Wang P, Wang D Abstract Macrophage-mediated inflammation plays a critical role in hypertensive kidney disease. Here we investigated the role of transient receptor potential ankyrin 1 (TRPA1), a sensor of inflammation, in angiotensin (Ang) II-induced renal injury. Subcutaneous infusion of Ang II (600ng/min/kg) for 28 days was used to induce hypertension and renal injury in mice. Results showed that Ang II-induced hypertensive mice have decreased renal Trpa1 expression (P<0.01) while Ang II receptor type 1a-deficient hypotensive mice have increased renal Trpa1 expression (P<0.05) compared with their normotensive counterparts. Ang II induced similar elevations of systolic blood pressure in Trpa1-/- and wild-type (WT) mice but led to higher levels of blood urea nitrogen (P<0.05), serum creatinine (P<0.05), and renal fibrosis (P<0.01) in Trpa1-/- mice than WT mice. Similarly, Ang II increased both CD68+/inducible nitric oxide synthase+ M1 and CD68+/arginase 1+ M2 macrophages in the kidney of both Trpa1-/- and WT mice (all P<0.01), with higher extents in Trpa1-/- mice (both P<0.01). Compared with WT mice, Trpa1-/- mice had significantly increased expression levels of inflammatory cytokines and their receptors in the kidney. Cultured murine macrophages were stimulated with phorbol 1...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research