Overview of Science and Mission
People Behind the Science
About the People
Kimm J. Hamann, Ph.D.
Research Interests and Summary
Programmed cell death is a critical mechanism in both physiological and pathological processes in human tissues. Therapeutic manipulation of cell death offers significant promise in controlling the onset and progression of many human diseases. A major area of research in Dr. Hamann's laboratory involves investigations of the roles and mechanisms of cell death, particularly apoptosis in ischemia/reperfusion cardiac injury. Studies here primarily center on the mitochondrion as a source of reactive oxygen species which play pivotal roles in cardiac cell death and survival and which function as intracellular initiators of apoptosis following oxidant stress. Key components of the apoptotic pathways are proteins called caspases, which can initiate and carry out the apoptotic death of cells. Dr. Hamann leads studies which focus on caspase-2 and other initiators, mediators, and regulators of apoptosis in cardiac myocytes.
Dr. Hamann also has begun new funded studies of the molecular mechanisms of protection induced by hypothermia. Dr. Hamann, in collaborations with other ERC members, Drs. Terry Vanden Hoek and David Beiser, has recently discovered molecular, cellular, and genomic evidence pointing to the Akt and p53 pathways as key targets of hypothermic modulation of cardiac cell death.
Additional research in Dr. Hamann's laboratory is also focused on cell death in leukemic cells, including both mitochondria and "death receptor" mediated pathways. Current studies also examine the role of the p53-related apoptosis-inducing protein complexes in programmed death of acute myelogenous leukemia cells.
For these and other studies, Dr. Hamann has been continuously funded by NIH since 1992 and currently holds two NIH R01s, "Mechanisms of Hypothermic Protection from Ischemia/reperfusion-induced Injury" (HL084643) and “Caspases & Oxidants: Initiation of Reperfusion-Induced Injury" (HL079641), both of which focus on molecular and cellular aspect of cardiac injury following ischemia and reperfusion.
Teaching and Service
Dr. Hamann has served as a regular member of the National Institutes of Health (NIH) study section "Myocardial Ischemia and Metabolism" (MIM) and as an ad hoc member on several other NIH review boards, including the "Cardiovascular & Renal" (CVB) and "Cell Development and Function" (CDF-5) study sections, various "Special Emphasis" panels, as well as review panels for the Heart and Stroke Foundation of Canada. He has recently served on the faculty of national and international scientific conferences such as the American Thoracic Society and the American Heart Association Scientific Sessions.
At the University of Chicago, Dr. Hamann routinely lectures on cell death in several undergraduate and graduate level courses. Dr Hamann has also directed an undergraduate course entitled "Animal Models of Human Disease." He currently directs a graduate course, "Cell Injury, Repair and Death," for the University's Committee on Molecular Medicine, of which he is a member. He also serves on several scientific and teaching committees at The University of Chicago and is currently the Director of Basic Science Research in the Emergency Resuscitation Center (ERC).
Selected Representative Publications
Zhao D, BS Abella, DG Beiser, JP Alvarado, H Wang, KJ Hamann, TL Vanden Hoek, LB Becker. Intra-arrest cooling with delayed reperfusion yields higher survival than earlier normothermic resuscitation in a mouse model of cardiac arrest. Resuscitation 77:242-249, 2008.
Shao ZH, WT Chang, KC Chan, KR Wojcik, CW Hsu, CQ Li, T Anderson, Y Qin, LB Becker, KJ Hamann* & TL Vanden Hoek.* Hypothermia induced cardioprotection using extended ischemia and early reperfusion cooling. Am J Physiol (Heart Circ Physiol) 292:H1995-2003, 2007. (*Co-senior authors)
Qin Y, Auh S, Blokh L, Long C, Gagnon I, Hamann KJ. TNF-a induces transient resistance to Fas-induced apoptosis in eosinophilic acute myeloid leukemia cells. Cell Molec Immunol 4:43-52, 2007.
Hamann, KJ, D Beiser & TL Vanden Hoek. Global cellular ischemia/reperfusion during cardiac arrest: Critical stress responses and the post-resuscitation syndrome. In: Cardiac Arrest-The Science and Practice of Resuscitation Medicine, 2nd ed., NA Paradis, et al., Eds., 2007.
Anderson TC, C-Q Li, Z-H Shao, T Hoang, KC Chan, KJ Hamann,* LB Becker,* TL Vanden Hoek.* Transient and partial mitochondrial inhibition for the treatment of post-resuscitation injury: getting it just right. (*Senior collaborating authors) Crit Care Medicine 34:S747-S482, 2006.
Lee RC, F Despa and KJ Hamann (Editors). Cell Injury: Mechanisms, Responses and Repair. New York Academy of Sciences, vol.1066, 2006. (Invited volume)
Qin Y, T Vanden Hoek, K Wojcik, CQ Li, ZH Shao, T Anderson, and KJ Hamann. Caspase-dependent cytochrome c release in reperfusion-induced apoptosis of ischemic chick cardiomyocytes. Amer. J. Physiol. (Heart Circ Physiol) 286:H2280-H2286, 2004.
Vanden Hoek T, Y Qin, K Wojcik, CQ Li, ZH Shao, T Anderson, LB Becker and KJ Hamann. Reperfusion, not simulated ischemia, initiates cytochrome c release and apoptosis injury in cardiomyocytes. Amer. J. Physiol. (Heart Circ Physiol) 284:H141-150, 2003.
Qin Y, B Camoretti-Mercado, L Blokh, CG Long,FD Ko and KJ Hamann. Fas resistance of leukemic eosinophils is due to activation of NF-kB by Fas ligation. J. Immunol. 169: 3536-3544, 2002.
Hamann KJ, JE Viera, AJ Halayko, D Dorscheid, SR White, SM Forsythe, B Camoretti-Mercado, KF Rabe and J Solway. Fas (CD95) crosslinking induces apoptosis in human airway smooth muscle cells. Am J Physiol 278:L618-624, 2000.
Hamann KJ, I Douglas and R Moqbel. Eosinophil mediators. In: Asthma and Rhinitis,
WW Busse and ST Holgate (eds), 2nd Edition, Blackwell Scientific Publications, pp. 394-428, 2000.