Lipid raft redox signaling platforms in endothelial dysfunction.
نویسندگان
چکیده
In response to various stimuli, membrane lipid rafts (LRs) are clustered to aggregate or recruit NADPH oxidase subunits and related proteins in vascular endothelial cells (ECs), forming redox signaling platforms. These LR signaling platforms may play important roles in the normal regulation of endothelial function and in the development of endothelial dysfunction or injury under pathological conditions. This LR-mediated mechanism now takes center stage in cell signaling for the regulation of many cellular activities or cell function such as ECs redox signaling, phagosomal activity of phagocytes, and cell apopotosis of lymphocytes. This brief review summarizes current evidence that relates to the formation of LR redox signaling platforms and their features in ECs, the functional significance of these signaling platforms in mediating death receptor activation-induced endothelial dysfunction, and the mechanisms initiating or promoting the formation of these platforms. It is expected that information provided here will help readers to understand this new signaling mechanism and perhaps extend the LR signaling platform concept to other research areas related to death receptors, redox signaling, endothelial biology, and cell/molecular biology of the cardiovascular system.
منابع مشابه
Critical role of lipid raft redox signaling platforms in endostatin-induced coronary endothelial dysfunction.
OBJECTIVE Endostatin (EST) was found to initiate a redox signaling cascade associated with activation of NADPH oxidase in endothelial cells (ECs). The present study tested whether EST stimulates clustering of ceramide-enriched lipid rafts (LRs), which assembles and activates NADPH oxidase to form redox signaling platforms. METHODS AND RESULTS Using confocal microscopy, we first demonstrated a...
متن کاملLipid raft clustering and redox signaling platform formation in coronary arterial endothelial cells.
Recent studies have indicated that lipid rafts (LRs) in the cell membrane are clustered in response to different stimuli to form signaling platforms for transmembrane transduction. It remains unknown whether this LR clustering participates in redox signaling in endothelial cells. The present study tested a hypothesis that clustering of LRs on the membrane of coronary endothelial cells produces ...
متن کاملContribution of lysosomal vesicles to the formation of lipid raft redox signaling platforms in endothelial cells.
We have demonstrated that the formation of lipid raft (LR)-redox signaling platforms membrane is associated with activation of acid sphingomyelinase (ASMase) in coronary arterial endothelial cells (CAECs). Given that the trafficking of lysosomal vesicles might play an essential role in ASMase activation, the present study tested whether lysosomal vesicles contribute to the formation of LR redox...
متن کاملAcid sphingomyelinase and its redox amplification in formation of lipid raft redox signaling platforms in endothelial cells.
This study examined the role of acid sphingomyelinase (ASM) and its redox amplification in mediating the formation of lipid raft (LR) redox signaling platforms in coronary arterial endothelial cells (CAECs). Using small interference RNA (siRNA) of ASM, Fas ligand (FasL)-induced increase in ASM activity, production of ceramide, and LR clustering in CAECs were blocked, and clustered Fas was also ...
متن کاملLipid raft redox signaling: molecular mechanisms in health and disease.
Lipid rafts, the sphingolipid and cholesterol-enriched membrane microdomains, are able to form different membrane macrodomains or platforms upon stimulations, including redox signaling platforms, which serve as a critical signaling mechanism to mediate or regulate cellular activities or functions. In particular, this raft platform formation provides an important driving force for the assembling...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Antioxidants & redox signaling
دوره 9 9 شماره
صفحات -
تاریخ انتشار 2007