Nadeem Goraya has always been interested in the intricacy and consistency of the vascular system, and considers himself blessed to be able to explore this interest under the guidance of Dr. Purdy. He has enjoyed the chance to pursue this animal-model project from the beginning through performing the analysis and probing for important proteins. He is thrilled to be a part of this project, with its potential significance in better understanding vascular function. Nadeem feels that his research experience has been a vital part of preparing for his ultimate goal of becoming a physician, and that the skills he has learned in the lab will help him remain well informed and productive throughout his career.

This study evaluated crucial contractile proteins and the role of vascular smooth muscle cell phenotype in the abdominal aorta of male Wistar rats exposed to simulated microgravity. Myofilament proteins myosin heavy chain (MHC), myosin light chain-20 (MLC20), and -actin were measured along with myofilament binding proteins calponin, h-caldesmon, and -tropomyosin, which are markers for phenotype change. Microgravity was simulated through use of the hind limb unweighting (HU) model for 20 days. Male Wistar rats, designated either HU or control (CTL) at random, were euthanized and the abdominal aortas were removed and stored for Western blot analysis. The aforementioned proteins were probed, and relative protein levels were quantified and compared between HU and CTL rats. Results indicate an HU-induced downregulation in all three contractile proteins, MHC, MLC20, and -actin. However, HU-induced upregulation of the myofilament binding, contraction inhibitory protein h-caldesmon was observed. No significant change was observed in either calponin or -tropomyosin. These results suggest that downregulation of contractile proteins and upregulation of the contraction inhibitory protein h-caldesmon could be possible mechanisms for HU-induced vasoconstrictor hyporesponsiveness.

Ralph E. Purdy School of Medicine

The UROP-sponsored research project carried out by Nadeem Goraya was an extraordinary, positive experience for both of us. I was able to provide a supportive environment in which Nadeem could learn techniques, discuss problems and ideas, delve into the literature, and undertake an exciting research project. On Nadeem’s side, his energy, initiative, imagination, and persistence were critical to his success. Nadeem’s study was the first to identify cellular mechanisms for the impairment of vasoconstriction and the resulting orthostatic intolerance experienced by astronauts and long-term bed rest patients. He found that microgravity can downregulate the expression of the very proteins involved in vasoconstriction, myosin and actin. Based on his work, we are now investigating mechanism-based therapeutic interventions.