PodcastNeovascularization

Science Signaling Podcast for 22 September 2015: SOCS3 prevents pathological retinal neovascularization

Sci. Signal.  22 Sep 2015:
Vol. 8, Issue 395, pp. pc24
DOI: 10.1126/scisignal.aad3734

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Abstract

This Podcast features an interview with Ye Sun and Lois Smith, authors of a Research Article that appears in the 22 September 2015 issue of Science Signaling, about how suppressor of cytokine signaling 3 (SOCS3) prevents retinal neovascularization in mice. Retinal neovascularization is the abnormal growth of blood vessels in the retina and a common cause of blindness in diabetics and preterm infants. Research suggests that crosstalk between the normal blood vessels that serve the retina and the neurons, glial cells, and photoreceptors that make up the retina drives retinal neovascularization. Sun et al. found that SOCS3 prevented oxygen-induced retinal neovascularization in mice because it keeps neural and glial cells of the hypoxic retina from releasing too much vascular endothelial growth factor (VEGF), a cytokine that stimulates blood vessel formation. SOCS3 reduced the production of VEGF in these cells by inhibiting activation of the transcription factor STAT3, an activator of vegfa expression.

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