PubMed · 12400471
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Bob Huff. 2002. Down in the lab.. https://pubmed.ncbi.nlm.nih.gov/12400471/
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Several studies have emphasized the relevance of dystrophin-associated protein complex (DAPC) to maintain the vascular function. Previously we postulated the presence of an utrophin associated protein complex (UAPC) in endothelium from umbilical cord vessels. In the present work, we demonstrate that utrophin (UTR) indeed forms a complex, with beta-dystroglycan (DG), epsilon-sarcoglycan (SG), caveolin-1 (cav-1), and endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells (HUVEC) by co-immunoprecipitation analysis. Additionally, we observed an increment in the protein levels of epsilon-SG, beta-DG, UTR and cav-1 after mechanical stretching. Interestingly, this stimulus also induced eNOS up-regulation, activation and release from the UAPC, and led to a significant increase in nitric oxide (NO) production. Finally, we propose that UAPC in HUVECs may play an important role in the regulation of vascular tone.
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One aspect of homocysteine (Hcy) action is the impairment of endothelial cell function due to an impairment of endothelial nitric oxide (NO) production. The activity of the endothelial isoform of NO synthase (eNOS) is regulated by its interaction with caveolin-1 (Cav-1). The aim of this study was to determine whether Hcy may alter the levels of Cav-1 and eNOS in endothelial caveolae. We isolated caveolae-enriched membrane fractions from Hcy-treated human coronary artery endothelial cells. We found that treatment with 500 microM Hcy for 6h significantly reduced the levels of Cav-1 and eNOS in caveolae compared to untreated control by 47+/-7% and by 38+/-14%, respectively. Similarly, long-term incubation (96h) of HCAEC with 100 microM Hcy led to a comparable effect. The decreased Cav-1 abundance in endothelial caveolae in response to Hcy resulted from a decrease in Cav-1 expression at the transcriptional level. The reduced levels of eNOS in caveolae were caused by a translocation of eNOS from the caveolar fractions to noncaveolar fractions. The effects of Hcy were associated with an impairment of stimulated release of NO. These results suggest that Hcy induced impairment of NO production through a modulation of Cav-1 expression associated with a loss of eNOS in caveolae.