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November 8, 2018 | 11:00 a.m. - 12:00 p.m.
Category: Seminar
Location: Scott Hall #3125 | Map
540 E. Canfield
Detroit, MI 48201
Cost: Free
Audience: Current Graduate Students, Faculty

Nicholas Sibinga, MD; Professor of Cardiology and of Developmental and Molecular Biology, Albert Einstein College of Medicine

“Controlling Metabolism in the Vascular Response to Injury”

ABSTRACT

Mitochondrial function is intimately involved in integrated growth-related processes such as development and tissue repair, and in homeostatic mechanisms that counteract aging and neurodegeneration, cardiovascular disease, and cancer. Physiologic mechanisms that control mitochondrial activity in such settings remain incompletely understood. In studies of the atypical cadherin FAT1, we found that it acts as a molecular ‘brake’ on mitochondrial respiration to regulate vascular smooth muscle cell (SMC) proliferation after arterial injury. Mechanistically, fragments of the FAT1 intracellular domain accumulate in SMC mitochondria, interact with multiple mitochondrial proteins, and modify respiratory function, including the activity of complexes I and II in the electron transport chain. SMCs lacking FAT1 grow faster, contain more aspartate, and consume more oxygen for ATP production, indicating that FAT1 function controls key regulators of cellular metabolism and growth. This surprising cadherin-based regulatory mechanism may be important in other settings of altered cell growth and metabolism.

For more information about this event, please contact Suzanne Shaw at 577-5325 or sshaw@wayne.edu.