Research ArticleAngiogenesis

The endothelial adaptor molecule TSAd is required for VEGF-induced angiogenic sprouting through junctional c-Src activation

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Science Signaling  19 Jul 2016:
Vol. 9, Issue 437, pp. ra72
DOI: 10.1126/scisignal.aad9256

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Disconnecting endothelial cells for new blood vessels

The endothelial cells lining blood vessels are linked together by adherens junctions, where VE-cadherin protein complexes must come apart so that endothelial cells can migrate and proliferate to form new blood vessels. This process is triggered by activation of the receptor VEGFR2, which stimulates the kinase c-Src. Gordon et al. showed that the adaptor protein TSAd linked these two signaling molecules in the developing trachea. TSAd recruited active c-Src to adherens junctions, which resulted in the breakdown of VE-cadherin complexes and enabled the rearrangement of endothelial cells to form a new blood vessel sprout. Because TSAd was required for blood vessel formation in developing trachea, but not in the developing retina, TSAd could be targeted to prevent abnormal vascular growth in a tissue-specific manner.

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