Vivek K. Vishnudas, Ph.D.
Postdoctoral Research Fellow

Education
University of Vermont, 2006

Lab
Jeffrey B. Miller

Research Interests
My primary focus has been to develop cell culture based models of Congenital Muscular Dystrophy (CMD) and FSH Dystrophy (FSHD) using patient derived primary cells. My most recent work demonstrates that differentiated laminin deficient human myoblasts that are plated on poly-lysine undergoes spontaneous apoptosis. The presence of laminin alpha 2 in the substrate is sufficient to prevent spontaneous apoptosis of these cells, suggesting that laminin alpha 2 deficiency triggers the activation of cell death signals. Apoptosis is considered to be an important component of CMD and understanding the mechanism of cell death in CMD is of vital importance. I have also been able to shed  light on the involvement of the Bax-Ku70 pathway in CMD and further the regulation of Bax-Ku70 pathway by deacetylase SIRT1. Similarly with the FSHD cells, I have been able to demonstrate that their sensitivity to pyruvate can be used as an important tool to delineate the pathological features of the disease. My future goal is to develop drug screens using patient derived laminin deficient and FSHD myoblasts. Taken together my research will generate useful information about pathological mechanisms in a diverse group of neuromuscular diseases and also provide a platform for testing drugs leading to ameliorative therapies.

Recent Publications
Girgenrath, M., Beermann, M. L., Vishnudas, V. K., Homma, S and Miller, J. B. (2009). "Pathology is alleviated by doxycycline in a laminin-alpha2-null model of congenital muscular dystrophy." Ann Neurol 65(1): 47-56.

Vishnudas, V.K and Miller, J.B. (2009)."Ku70 mediates Bax dependent pathogenesis in laminin- alpha2- deficient human muscle cells and mouse models of  congenital muscular dystrophy." Hum Mol Genet. Published online: Aug 19, doi: 10.1093/hmg/ddp399

Contact Details:
email: vishnudas@bbri.org, tel. 617-658-7725