Insulin-like growth factor-1 (IGF-1) is commonly associated with diabetes and cancer, but the new study suggests a broader role related to neurodegenerative disorders, said Benxu Cheng, Ph.D., lead author of the paper in the journal Molecular and Cellular Neuroscience. Dr. Cheng is assistant professor of cellular and structural biology at the UT Health Science Center and is located at the Regional Academic Health Center (RAHC) Medical Research Division in Edinburg.
IGF-1 is critical for the survival of neurons, the brain cells that die in these diseases. IGF-1 protects cells against different kinds of stressors, said Shivani Maffi, Ph.D., assistant professor of molecular medicine and director of the Optical Imaging Core at the RAHC Medical Research Division.
In the study, cells pretreated with IGF-1 fared better than untreated cells when exposed to a toxin called epoximicin. This toxin induces neurodegeneration similar to that seen in Alzheimer’s and Parkinson’s diseases. IGF-1 apparently works by sending signals that help proteins perform intracellular quality control.
At the time of its dedication in 2006, the RAHC Medical Research Division was the first biomedical research facility of its type on the Texas-Mexico border. The new paper is the latest fruit of science conducted in the building, which is adjacent to The University of Texas-Pan American in the Lower Rio Grande Valley. “We want to highlight that a lot of the IGF-1 work was carried out in the Valley at this campus,” Dr. Maffi said.
The paper’s senior author, James Roberts, Ph.D., is a professor at Trinity University in San Antonio and is a research professor of pharmacology at the Health Science Center.
Benxu Cheng, Shivani Kaushal Maffi, Alex Anthony Martinez, Yolanda P. Villarreal Acosta, Liza D. Morales, James L. Roberts, Insulin-like growth factor-I mediates neuroprotection in proteasome inhibition-induced cytotoxicity in SH-SY5Y cells, Molecular and Cellular Neuroscience, In Press, Uncorrected Proof, Available online 23 April 2011, ISSN 1044-7431, DOI: 10.1016/j.mcn.2011.04.002.
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