Dr. Ian Bird Receives Grant
Published: 3/31/2011





Ian Bird
Dr. Ian Bird has recently been notified by NIH that he will be the recipient of an NIH R21 - Translational Research in Pediatric and Obstetric Pharmacology award. Dr. Bird is the Principal Investigator and Dr. Dinesh Shah is the Co-Investigator. The project "Vascular Endothelial Dysfunction in Preeclampsia" is funded for $275,000 over a 2 year time period.

Their intent is to establish if it is possible to use HUVEC from PE subject as suitable cells through a specific drug screen with the following specific aims in mind:

1. SpAim 1: Hypothesis: The observed sustained [Ca2+]i bursts in responses to ATP in intact UV Endo from normal pregnancy are due to TRPC3 and CX43 activation, and losses of Ca2+ burst associated with strategies aimed at TRPC3 or CX43 inhibition replicate the lower/blunted Ca2+ and NO responses seen in PE subjects.

2. SpAim 2 (Transitional to Aim 3): Hypothesis: PE associated dysfunction in PE derived UV Endo or PE derived HUVEC (passage 3) compared to that from normal subjects is not due to simple changes in the relative levels of expression of P2Y2 receptors, G proteins, PLC, IP3 receptors, TRPC channels, or connexins.

3. SpAim 3: Hypothesis: In short term culture, the sustained [Ca2+]i burst responses to ATP in HUVEC from normal pregnancy due to CX43 potentiation of IP3 sensitive TRPC3 activation are retained, and are lacking in cells derived from PE subjects. Further, inhibition of either IP3 mediated TRPC3 activation or CX43 mediated cell-cell communication in HUVEC from normal subjects replicates the loss of function seen in HUVEC from PE subjects, but does not further inhibit the function of HUVEC from PE subjects.