The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension.

The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension. Am J Physiol Renal Physiol. 2016 Apr 6;:ajprenal.00040.2016 Authors: Weiss S, Rosendahl A, Czesla D, Meyer-Schwesinger C, Stahl RA, Ehmke H, Kurts C, Zipfel PF, Köhl J, Wenzel UO Abstract Adaptive and innate immune responses contribute to hypertension and hypertensive end-organ damage. Here we determined the role of the anaphylatoxin C5a, a major inflammatory effector of the innate immune system that is generated in response to complement activation, in hypertensive end-organ damage. For this pupose we assessed the phenotype of C5a receptor 1 (C5aR1)-deficient mice in in angiotensin II (Ang II)-induced renal and cardiac injury. Expression of the C5aR1 on infiltrating and resident renal as well as on cardiac cells was determined using a GFP-C5aR1 reporter knock-in mouse. Flow cytometric analysis of leukocytes isolated from the kidney of GFP-C5aR1 reporter mice showed that 28% of CD45+ cells expressed C5aR1. Dendritic cells were identified as the major C5aR1 expressing population (88.5%) followed by macrophages and neutrophils. Using confocal microscopy we detected C5aR1 in the kidney mainly on infiltrating cells. In the heart only infiltrating cells stained C5aR1 positive. To evaluate the role of C5aR1- deficiency in hypertensive injury an aggravated model of hypertension was used. Unilateral nephrectomy was perfor...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research