EphrinB2 controls vessel pruning through STAT1-JNK3 signalling

Ombretta Salvucci, Hidetaka Ohnuki (), Dragan Maric, Xu Hou, Xuri Li, Sung Ok Yoon, Marta Segarra, Charles G. Eberhart, Amparo Acker-Palmer and Giovanna Tosato ()
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Ombretta Salvucci: Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health
Hidetaka Ohnuki: Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health
Dragan Maric: National Institutes of Neurological Disorders and Stroke, National Institutes of Health
Xu Hou: National Eye Institute, National Institutes of Health
Xuri Li: National Eye Institute, National Institutes of Health
Sung Ok Yoon: Ohio State University
Marta Segarra: Institute of Cell Biology and Neuroscience and BMLS, Goethe University Frankfurt
Charles G. Eberhart: Ophthalmology and Oncology, Johns Hopkins University
Amparo Acker-Palmer: Institute of Cell Biology and Neuroscience and BMLS, Goethe University Frankfurt
Giovanna Tosato: Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health

Nature Communications, 2015, vol. 6, issue 1, 1-17

Abstract: Abstract Angiogenesis produces primitive vascular networks that need pruning to yield hierarchically organized and functional vessels. Despite the critical importance of vessel pruning to vessel patterning and function, the mechanisms regulating this process are not clear. Here we show that EphrinB2, a well-known player in angiogenesis, is an essential regulator of endothelial cell death and vessel pruning. This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1. JNK3 activation causes endothelial cell death. In the absence of JNK3, hyaloid vessel physiological pruning is impaired, associated with abnormal persistence of hyaloid vessels, defective retinal vasculature and microphthalmia. This syndrome closely resembles human persistent hyperplastic primary vitreus (PHPV), attributed to failed involution of hyaloid vessels. Our results provide evidence that EphrinB2/STAT1/JNK3 signalling is essential for vessel pruning, and that defects in this pathway may contribute to PHPV.

Date: 2015
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DOI: 10.1038/ncomms7576

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