Nihar Nayak, Ph.D., D.V.M.
Academic Appointments
- Assistant Professor, Obstetrics & Gynecology
- Member, Bio-X
- Member, Child Health Research Institute
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 723-0953Alternate Contact Tracy Lindsay AA Email Tel Work (650) 498-7408
Professional Overview
Honors and Awards
- 2011 Vision Grant Award, presented at the Annual Gala 'Saving Grace - A Night of Hope and Gratitude', Preeclampsia Foundation (2011)
- Building Interdisciplinary Research Careers in Women's Health (BIRCWH) Award, NIH (2004-2008)
- Junior Investigator Award, Andrew W. Mellon Foundation (2000-2004)
- Burroughs Wellcome Fund Travel Fellow, Society for the Study of Reproduction (1999)
- Travel Grant Award, Endocrine Society (1999)
Professional Education
| Postdoctoral Fellowship: | ONPRC, Oregon, USA, Reproductive Sciences (2000) |
| PhD: | AIIMS, New Delhi, Reproductive Physiology (1998) |
| MVSc: | Orissa Univ of Agril and Tech, Veterinary Physiology (1989) |
| BVSc & AH: | Orissa Univ of Agril and Tech, Veterinary Medicine (1986) |
Scientific Focus
Current Research Interests
Research in my laboratory is focused on understanding the mechanisms of endometrial angiogenesis and vascular remodeling during the menstrual cycle and pregnancy. We are particularly interested in understanding the mechanisms of spiral artery growth and remodeling in the primate uterus. These arteries are unique to the primate endometrium. They develop from the radial arteries of the myometrium and course through the endometrium, where they develop their coiled structure and vascularize primarily the upper endometrial zones. Their growth is primarily driven by progesterone in the luteal phase of the menstrual cycle and pregnancy. At the end of a nonfertile cycle, when progesterone levels fall, the spiral arteries severely constrict, leading to ischemia of the upper endometrial zones and menstrual breakdown of endometrium. During pregnancy, the trophoblasts invade the spiral arteries and replace the internal lining of these arteries, thereby regulate the vascular resistance and blood flow to the placenta and fetus. The degree of trophoblast invasion into these arteries appears to be a major determinant of pregnancy outcome. Inadequate invasion, particularly restricted endovascular invasion of spiral arteries, has been implicated in the pathophysiology of preeclampsia, preterm labor, and intrauterine growth restriction (lUGR). We believe that most of the pregnancy-related vascular complications manifested late in gestation, including preeclampsia, have their origins early in pregnancy. Our main goal is to identify the abnormalities in implantation that may lead to various pregnancy-related vascular complications.
Publications
- Dynamic regulation of wnt7a expression in the primate endometrium: implications for postmenstrual regeneration and secretory transformation. Endocrinology. 2012; (3): 1063-9
- Decreased circulating soluble Tie2 levels in preeclampsia may result from inhibition of vascular endothelial growth factor (VEGF) signaling. J Clin Endocrinol Metab. 2011; (7): E1148-52
- Noninvasive monitoring of placenta-specific transgene expression by bioluminescence imaging. PLoS One. 2011; (1): e16348
- Soluble receptor-mediated selective inhibition of VEGFR and PDGFRbeta signaling during physiologic and tumor angiogenesis. Proc Natl Acad Sci U S A. 2008; (29): 10185-90
- VEGF blockade inhibits angiogenesis and reepithelialization of endometrium. FASEB J. 2008; (10): 3571-80
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