Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney - PubMed (original) (raw)

doi: 10.1038/hr.2011.23. Epub 2011 Mar 31.

Affiliations

PMID: 21451526
DOI: 10.1038/hr.2011.23

Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney

Kazuaki Shimizu et al. Hypertens Res. 2011 Jun.

Abstract

Hypertension promotes and escalates kidney injury, including kidney fibrosis. Fractalkine/CX3CL1 is a unique chemokine that works as a leukocyte chemoattractant and an adhesion molecule. Recently, fractalkine/CX3CL1 has been reported to promote tissue fibrosis via its cognate receptor, CX3CR1. However, the involvement of the fractalkine-CX3CR1 axis in the pathogenesis of hypertensive kidney fibrosis remains unclear. The impacts of the fractalkine-CX3CR1 axis on hypertensive kidney fibrosis were investigated in a deoxycorticosterone acetate (DOCA)-salt hypertensive model in CX3CR1-deficient mice, which were sacrificed on day 28. The blood pressure levels were similarly elevated in both CX3CR1-/- C57BL/6 and wild-type C57BL/6 mice. Fractalkine and CX3CR1 were upregulated in kidneys that were damaged by hypertension. Deficiency in CX3CR1 inhibited kidney fibrosis, as evidenced by a decrease in the presence of interstitial fibrotic area detected by type I collagen in Mallory-Azan staining, concomitant with the downregulation of transforming growth factor (TGF)-β(1) and type I procollagen mRNA expression in damaged kidneys. The CX3CR1 blockade also decreased the number of infiltrating F4/80-positive macrophages in damaged kidneys. These results suggest that the fractalkine-CX3CR1 axis contributes to kidney fibrosis in a hypertensive mouse model, possibly by the upregulation of macrophage infiltration and the expression of TGF-β(1) and type I collagen.

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Fractalkine and its receptor, CX3CR1, promote hypertensive interstitial fibrosis in the kidney - PubMed (original) (raw)