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First published online January 24, 2007
doi: 10.1242/10.1242/jcs.03361

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Nitric oxide promotes endothelial cell survival signaling through S-nitrosylation and activation of dynamin-2

Ningling Kang-Decker^1,*, Sheng Cao^1,*,, Suvro Chatterjee¹, Janet Yao¹, Laurence J. Egan¹, David Semela¹, Debabrata Mukhopadhyay² and Vijay Shah^1,

¹ GI Research Unit, Department of Physiology and Tumor Biology Program, Mayo Clinic, Rochester, MN 55903, USA
² Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55903, USA

Authors for correspondence (e-mail: cao.sheng{at}mayo.edu; shah.vijay{at}mayo.edu)

Accepted 20 November 2006

Endothelial cell-based angiogenesis requires activation of survival signals that generate resistance to external apoptotic stimuli, such as tumor necrosis factor-alpha (TNF-), 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--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--induced apoptosis and nitric oxide-dependent survival signals, with implications highly relevant to angiogenesis.

Key words: Endocytosis, Apoptosis, Angiogenesis

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