4.7 Article

Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis

Journal

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 29, Issue 1, Pages 168-181

Publisher

AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2017050544

Keywords

-

Funding

  1. Medical Research Council of the United Kingdom [MR/L020254/1, MR/J006742/1]
  2. National Natural Science Foundation of China [NSFC 81170644]
  3. Visiting Scholarship of Xi'an Jiaotong University
  4. Medical Research Council [G0600892, MR/R010757/1, MR/L020254/1, MR/M012263/1, MR/J006742/1] Funding Source: researchfish
  5. National Institute for Health Research [NF-SI-0510-10142] Funding Source: researchfish
  6. MRC [MR/M012263/1, G0600892, MR/R010757/1, MR/L020254/1] Funding Source: UKRI

Ask authors/readers for more resources

Collectin-11 is a recently described soluble C-type lectin, a pattern recognition molecule of the innate immune system that has distinct roles in host defense, embryonic development, and acute inflammation. However, little is known regarding the role of collectin-11 in tissue fibrosis. Here, we investigated collectin-11 in the context of renal ischemia-reperfusion injury. Compared with wild-type littermate controls, Collec11 deficient (CL-11(-/-)) mice had significantly reduced renal functional impairment, tubular injury, renal leukocyte infiltration, renal tissue inflammation/fibrogenesis, and collagen deposition in the kidneys after renal ischemia-reperfusion injury. In vitro, recombinant collectin-11 potently promoted leukocyte migration and renal fibroblast proliferation in a carbohydrate-dependent manner. Additionally, compared with wild-type kidney grafts, CL-11(-/-) mice kidney grafts displayed significantly reduced tubular injury and collagen deposition after syngeneic kidney transplant. Our findings demonstrate a pathogenic role for collectin-11 in the development of tubulointerstitial fibrosis and suggest that local collectin-11 promotes this fibrosis through effects on leukocyte chemotaxis and renal fibroblast proliferation. This insight into the pathogenesis of tubulointerstitial fibrosis may have implications for CKD mediated by other causes as well.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available