VEGFR2 is activated by high-density lipoproteins and plays a key role in the proangiogenic action of HDL in ischemia

Carla M. Cannizzo, Aaron A. Adonopulos, Emma L. Solly, Anisyah Ridiandries, Laura Z. Vanags, Jocelyne Mulangala, Sui Ching G. Yuen, Tania Tsatralis, Rodney Henriquez, Stacy Robertson, Stephen J. Nicholls, Belinda A. Di Bartolo, Martin K. C. Ng, Yuen Ting Lam, Christina A. Bursill, Joanne T. M. Tan
  • The FASEB Journal, January 2018, Federation of American Societies For Experimental Biology (FASEB)
  • DOI: 10.1096/fj.201700617r

What is it about?

Cardiovascular disease is a condition that involves the heart and blood vessels and is linked to the build up of fatty deposits in the arteries, which can lead to narrowing or complete blockage, reducing blood flow to the tissue. New blood vessel formation is an important process that allows the body to bypass a blocked vessel and promote the return of blood flow to tissues. We have previously shown that HDL (the "good" cholesterol) can help new blood vessels grow by increasing levels of a key protein called VEGFR2. VEGFR2 itself plays a key role in new blood vessel formation as it can be activated and then turn on other tissue survival processes. This study sought to: (1) explore the effects of HDL on VEGFR2 activation and other proteins and (2) determine if VEGFR2 is important in controlling the ability of HDL to grow new blood vessels. We found that HDL increases activation of VEGFR2 and two other important proteins. When VEGFR2 was blocked, HDL can no longer grow new blood vessels. This has the potential to address health concerns linked to diseases where new blood vessel formation is critical including heart disease, stroke and peripheral vascular disease.

The following have contributed to this page: Dr Joanne TM Tan

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