C. Michael Crowder, M.D., Ph.D.

  • Alan J. Treuer Endowed Professor of Anesthesiology and Pain Medicine
  • Chairman Department of Anesthesiology and Pain Medicine
  • Adjunct Professor of Genome Sciences

Research Interests

Hypoxia, whether neuronal or myocardial, is the most severe anesthetic complication and one for which anesthesiologists have little treatment when it occurs. My long term goal is to develop a better understanding of the biology of hypoxic cellular injury. My hope is that this improved understanding will contribute to the development of effective therapies to rescue neurons and cardiac myocytes injured by hypoxia and ischemia. We have taken a patient, long term, unbiased genetic screening approach to this problem because of the difficulty thus far of developing effective therapies from our existing knowledge. My lab combines techniques in genetics, molecular biology, cell biology, and biochemistry using C. elegans as our primary model system. I have a broad expertise gained from my graduate training in medicine and molecular neurobiology and my postdoctoral training in C. elegans genetics. Current projects in my laboratory revolve around defining the role of protein homeostasis in hypoxic cellular injury. Protein homeostasis is a burgeoning field that has in my view been under-studied for its role in hypoxic injury. C. elegans has a considerable set of genetic and cell biological tools to bring to bear on this question. We have also incorporated testing of the role of proteostasis in the survival of primary mouse neurons using gene knockdown and drugs. 

Selected Publications

  • Scott BA, Sun C-L, Mao X, Yu C, Vohra B, Milbrandt J, Crowder CM. Role of oxygen consumption in hypoxia protection by translation factor depletion. Journal of Experimental Biology 216(12):2283-92, 2013
  • Mao XR, Crowder CM. Protein misfolding induces hypoxic preconditioning via a subset of the unfolded protein response machinery. Mol Cell Biol 30(21):5033-42, 2010.
  • Anderson LL, Mao X, Scott BA, Crowder CM. Survival from hypoxia by inactivation of aminoacyl-tRNA-Synthetases. Science 2009 323: 630-33.
  • Mabon ME, Mao X, Jiao Y, Scott BA, Crowder CM. Systematic identification of gene activities promoting hypoxic death. Genetics 2009 181:483-96.
  • Mabon ME, Scott BA, Crowder CM. Divergent mechanisms controlling hypoxic sensitivity and lifespan by the DAF-2/Insulin/IGF-Receptor Pathway. PLOS One 2009 4:e7937.
  • Samokhvalov V, Scott BA, Crowder CM. Autophagy protects from hypoxic injury in C. elegans. Autophagy 4:1034-41, 2008.
  • Dasgupta N, Patel A, Scott BA, Crowder CM. Hypoxic Preconditioning requires the Apoptosis Protein CED-4 in C. elegans. Current Biology 2007 17:1954-1959.
  • Scott BS, Avidan M, Crowder CM. Regulation of hypoxic death in C. elegans by the insulin/IGF receptor homolog DAF-2. Science 2002 296:2388-2391.