Ohio University graduate student Amrita Basu won second place in the poster presentation competition at the second annual Appalachian Regional Cell Conference (ARCC) in Charleston, WV, in October.
Her poster, co-authored with Dr. John Kopchick, was on “Quantitative Analysis of Gene Expression in the Brain of Transgenic bGH and Wild Type Mice.” Basu is a student in the Molecular and Cellular Biology Graduate Program at Ohio University. Her research was on growth hormone and neurodegenerative diseases.
Abstract: The presence of growth hormone (GH) and GH receptor (GHR) in various regions of the mammalian brain as observed in experimental and/or physiological alteration of GH signaling [e.g. acromegaly (increased GH action), dwarfism (reduced GH action) and Laron Syndrome (disrupted GH signaling due to non-functional GHR)], indicate possible involvement of GH in development and function of the central nervous system, e.g. neuronal proliferation, cognition, memory and aging. Comprehensive understanding of GH function in the brain, as a diabetogenic hormone (due to anti-insulin action) and primary regulator of insulin like growth factor-1 (IGF-1) production, will help in elucidating role of GH in normal brain and in Alzheimer’s disease (AD), a neurodegenerative disease associated with perturbed glucose metabolism and insulin/IGF-1 signaling in the brain. The present study aimed at quantitative estimation of eight genes (GH, GHR, IGF-1, IGF-1 receptor, insulin, insulin receptor, monoamine oxidase (MAO) A and B) in six months old, male, transgenic giant bovine growth hormone (bGH) mice (model of acromegaly) compared to wild type littermates. Following total RNA isolation, cDNA synthesis, quantitative real time polymerase chain reaction (qPCR) and data analysis, up-regulated expression of GH and IGF-1 and down-regulation of GHR, IGF-1 receptor, insulin, insulin receptor, MAO-A and MAO-B mRNA transcript abundance were observed in various brain regions in bGH mice, relative to controls. Further proteomic analysis of the brain tissue of these animals will be performed for a better understanding of the molecular effect of GH in the brain and to identify potential therapeutic targets in GH signaling pathway, relevant to AD and other neuronal diseases. This work was supported in part by the State of Ohio’s Eminent Scholar Program that includes a gift from Milton and Lawrence Gall, by the AMVETS, by the Diabetes Research Initiative at Ohio University, and by NIH grants DK083729, AG031736.
Comments