e-mail- plsingh@med.wayne.edu

Education and Training:
B. Sc. 1982, Biology & Chemistry, D M College of Science, Imphal, India
M.Sc. 1984, Zoology, Cell Biology, Gujarat University, Ahmedabad, India
Ph.D. 1991, Biochemistry, Indian Institute of Science, Bangalore, India
Research Fellow, 1991-1992, Neuropathology, Ohio State University, Columbus, OH
Research Postdoctoral Fellow, 1992-1996, Department of Biochemistry, The University of Mississippi Medical Center, Jackson
Senior Research Associate, 1996 -1997, Department of Medicine, The University of Mississippi Med. Center, Jackson
Visiting Scientist, Jul 7-11, 2003, NIH, Bethesda, MD, Proteomics Research at NHLBI and NIDDK

Professional and Faculty Appointments:
Instructor, 1997- 2001, Department of Medicine, The University of Mississippi Medical Center, Jackson, MS
Assistant Professor (Research), 2001-2005, Departments of Internal Medicine and Physiology, Wayne State University School of Medicine, Detroit, MI
Assistant Professor, 2005-present, Departments of Anatomy/Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, MI

Major Research Interests:
To understand the molecular basis for endothelial cell dysfunction and leakage of retinal blood vessels in diabetes; Targeted genomics and proteomics-based identification of early biomarkers of diabetes and its vascular complications of the eyes and kidney – glycoproteomics; Therapeutic approaches to prevent/slow down the development and progression of diabetic retinopathy/nephropathy.

Current Research:
Diabetes mellitus is a long-term devastating disease, which affects numerous cellular and molecular processes leading to organ failure. Diabetes is also the number one cause of blindness and renal failure among the working adults in the US and around the globe. Our laboratory is interested in understanding (i) the molecular mechanism of excess extracellular matrix (ECM) accumulation in the diabetic glomerular mesangium and (ii) alterations in the expression of ECM/adhesion molecules in retinal endothelial cells and blood retinal barrier breakdown in diabetic retinopathy. Chronic hyperglycemia leads to increased cellular oxidative stress and glucose metabolic flux through the hexosamine biosynthetic pathway (HBP, which generates amino sugars for glycoproteins, glycolipids and glycans) and induces the expression of several inflammatory growth factors/cytokines. How does oxidative stress, HBP flux and growth factors (IGF-1, VEGF, TGF-b1) alter ECM/Adhesion molecule expression at the transcriptional level and post-translation modifications (e.g., glycosylation) and intracellular signaling mechanisms are being investigated? We use several cellular and STZ-induced diabetic animal models to answer some of these important questions. Genomic (microarray) and proteomic (2D gel/Mass Spectrometry) approaches as well as biochemical and molecular biology methods are employed.

Research Support:
American Diabetes Association Career Development Award
Robert Schrier Young Investigator Award of the National Kidney Foundation