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Nephron Exp Nephrol. 2012;120(1):e20-31. doi: 10.1159/000332026. Epub 2011 Nov 25.

Vascular endothelial cadherin modulates renal interstitial fibrosis.

Author information

1
Department of Pediatrics, University of Washington, Seattle, WA 98101-1309, USA. ikuyo.yamaguchi@seattlechildrens.org

Abstract

BACKGROUND/AIMS:

Renal interstitial fibrosis is a final common pathway of all chronic, progressive kidney diseases. Peritubular capillary rarefaction is strongly correlated with fibrosis. The adherens junction protein vascular endothelial cadherin (VE-cadherin) is thought to play a critical role in vascular integrity. We hypothesized that VE-cadherin modulates the renal microcirculation during fibrogenesis and ultimately affects renal fibrosis.

METHODS:

Unilateral ureteral obstruction (UUO) was used as a renal fibrosis model in VE-cadherin heterozygote (VE+/-) and wild-type (WT) mice, and the kidneys were harvested at days 3, 7, and 14. Peritubular capillary changes and fibrogenesis were investigated.

RESULTS:

VE+/- mice had lower levels of VE-cadherin protein than WT mice at 3 and 7, but not 14 days after UUO. Vascular permeability was significantly greater in VE+/- mice 7 days after UUO, while peritubular capillary density was not significantly different in VE+/- and WT mice. Interstitial myofibroblast numbers and collagen I and III mRNA levels were significantly higher in VE+/- mice, consistent with a stronger early fibrogenic response. Expression of the pericyte marker neuron-glial antigen 2 was upregulated after UUO, but was not greater in VE+/- mice compared to the WT mice.

CONCLUSION:

Our data suggest that VE-cadherin controls vascular permeability and limits fibrogenesis after UUO.

PMID:
22126970
PMCID:
PMC3254033
DOI:
10.1159/000332026
[Indexed for MEDLINE]
Free PMC Article

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