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Formation of Lipid Raft Redox Signaling Platforms in Glomerular Endothelial Cells: An Early Event of Homocysteine‐Induced Glomerular Injury

We have demonstrated that the formation of lipid raft (LR)‐redox signaling platforms on the cell membrane serves as an important transmembrane signaling mechanism in endothelial cells. We wondered whether this LR signaling platforms participate in redox signaling induced by hyperhomocysteinemia in rat glomerular endothelial cells (GECs). The present study tested the hypothesis that homocysteine (Hcys) induces LRs clustering on the membrane of GECs and form a redox signaling platform by aggregation and activation of NAD(P)H oxidase subunits. By confocal microscopic analysis, we found that incubation of GECs with Hcys for 30 min not only stimulated the clustering and trafficking of individual LRs on the plasma membrane of GECs, but also induced NAD(P)H oxidase membrane‐associated subunit gp91phox(Nox‐2) aggregation. In addition, p47phox, a crucial cytosolic subunit and Rac GTPase were found translocated into LR clusters. This aggregation or translocation was substantially blocked by nystatin and methyl‐ß‐cyclodextrin (MCD), two compounds for disruption of LRs. Correspondingly, superoxide (O2−.) production induced by Hcys was decreased by 52% in the presence of MCD, as measured by ESR spectrometry. These results suggest that Hcys can induce the formation of LR redox signaling platform in GECs even at an early stage of its action, which may represent an early event of Hcys‐induced glomerular injury