Premium
Caveolin‐1 knockout mice have decreased enrichment of redox‐sensitive enzymes in renal caveolar fractions
Author(s) -
Jennings Michelle May,
Roth David M,
Insel Paul A,
Patel Hemal H
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1424-c
Subject(s) - caveolae , caveolin 1 , reactive oxygen species , kidney , chemistry , caveolin , knockout mouse , nitric oxide , microbiology and biotechnology , superoxide dismutase , biochemistry , biology , signal transduction , enzyme , endocrinology , receptor , organic chemistry
Acute kidney injury (AKI) is associated with generation of reactive oxygen species (ROS). Caveolae are cholesterol‐, sphingolipid‐, and caveolin‐ enriched membrane microenvironments. They have enriched expression of various signaling molecules, a subset of which include redox‐sensitive enzymes. Caveolin‐1 knock out mice have impaired renal calcium reabsorption in addition to altered nitric oxide signaling, endothelial vasoactive and transport function, all of which could impact renal function in AKI. We hypothesize that caveolae help protect the kidney by buffering ROS through enrichment of redox sensitive enzymes that lower levels of ROS. Whole kidney lysates are highly enriched in caveolin‐1 and ‐2 but do not express caveolin‐3. Kidney lysates prepared from caveolin‐1 knockout mice lack expression of caveolin‐1 and have significantly lower expression of caveolin‐2, suggesting a loss of caveolae formation. Whole kidney lysates subjected to sucrose density fractionation from wild‐type animals, but not caveolin‐l knockout mice, have enrichment of superoxide dismutase, ferritin, glutathione peroxidase, and endothelial nitric oxide synthase in buoyant caveolar fractions. These results suggest that caveolae in the kidney are sites of localization of ROS buffering enzymes that may play a protective role during acute kidney injury.