Abstract:
:Endothelial cell-based angiogenesis requires activation of survival signals that generate resistance to external apoptotic stimuli, such as tumor necrosis factor-alpha (TNF-alpha), during pathobiologic settings. Mechanisms by which this is achieved are not fully defined. Here, we use a model in which the multifunctional cytokine nitric oxide counterbalances TNF-alpha-induced apoptosis, to define a role for membrane trafficking in the process of endothelial cell survival signaling. By perturbing dynamin GTPase function, we identify a key role of dynamin for ensuing downstream endothelial cell survival signals and vascular tube formation. Furthermore, nitric oxide is directly demonstrated to promote dynamin function through specific cysteine residue nitrosylation, which promotes endocytosis and endothelial cell survival signaling. Thus, these studies identify a novel role for dynamin as a survival factor in endothelial cells, through a mechanism by which dynamin S-nitrosylation regulates the counterbalances of TNF-alpha-induced apoptosis and nitric oxide-dependent survival signals, with implications highly relevant to angiogenesis.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Kang-Decker N,Cao S,Chatterjee S,Yao J,Egan LJ,Semela D,Mukhopadhyay D,Shah Vdoi
10.1242/jcs.03361subject
Has Abstractpub_date
2007-02-01 00:00:00pages
492-501issue
Pt 3eissn
0021-9533issn
1477-9137pii
120/3/492journal_volume
120pub_type
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