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Discordant regulation of preproenkephalin gene expression in different models of rat heart hypertrophy
	Boluyt MO, O'Neill L, Zheng JS, Meredith AL, Lakatta EG, Crow MT.
The transition from stable compensated hypertrophy to heart failure in rats with long-term aortic constriction.
	Boluyt MO, Meredith AL, O'Neill L, Crow MT, Lakatta EG, Brooks WW, Bing OHL, Conrad CH.
Adrenergic influences on rat cardiac hypertrophy in vivo.
	Boluyt MO, O'Neill L, Baker SP, Pitha J, Crow MT, Lakatta EG.
Basal but not elevated MAPK activity is required for cardiac myocyte hypertrophy.
	Boluyt MO, Heckendorf LA, Vieyra ER, Liu Y, Pineyro M, O'Neill L, Sollott SJ, Crow MT, Lakatta EG, Younes A.
Age effects on competitive physical performance.
	Boluyt MO, Dennison CS.
The p70 S6 kinase signaling pathway is activated in rat heart by an acute bout of exercise.
	Scalia AF, Reichbach M, Boluyt MO.
Activation of p70 S6 kinase in left ventricle of miniature swine after exercise and coronary artery occlusion.
	Loyd AM, Korzick DH, Laughlin MH, Boluyt MO.
Proteome Mapping of Heart Failure in Aging
	Boluyt MO (PI) , Andrews P, Hanash, S
	ABSTRACT: Heart failure is a major health problem in the elderly. Evidence indicates that a cardiac aldosterone signaling system plays an important role in the fibrosis associated with heart failure. Spironolactone, an aldosterone receptor antagonist, counteracts some of the effects of aldosterone in culture and in vivo. Aldosterone exerts its effects in target cells by binding to the mineralocorticoid receptor (MR) and stimulating transcription of effector genes. According to this paradigm, increases in fibrosis can be explained by the action of the aldosterone-MR complex on cardiac fibroblast genes that encode extracellular matrix proteins. A number of observations are not explained by this paradigm, however, including our preliminary data suggesting that spironolactone treatment of old rats does not decrease fibrosis as predicted, but increases the collagen content of the heart. Another paradoxical finding is that conditonal suppression of MR expression in cardiac myocytes of transgenic mice leads to fibrosis and heart failure. Emerging evidence strongly suggests that rapid non-genomic effects of aldosterone may explain some of the confusion, but the mechanisms by which these non-genomic effects are enacted have been elusive. The specific aims of this proposal are to identify novel protein mediators of aldosterone action that may regulate the age-associated increases in fibrosis and to identify novel proteins that interact with aldosterone and/or the MR to account for the non-genomic effects of aldosterone. We will study existing heart tissue samples from young and old rats treated chronically with vehicle or spironolactone. We will also generate cardiac myocyte and cardiac fibroblast cell populations from isolated hearts of old rats perfused briefly with vehicle or aldosterone. Proteins from cytosolic and particulate fractions of each cell type will be prepared for proteomic analyses. 2-D gel electrophoresis will be employed to identify differentially expressed or posttranslationally modified proteins. We will target proteins involved in the aldosterone signaling system by immunoprecipitation of MR-associated proteins. These studies are expected to identify novel proteins that may mediate the effects of aldosterone in the aged failing heart. Identification of proteins involved in aldosterone signaling will lead to the development of new hypotheses for future grant proposals addressing their roles in the development of heart failure in the elderly.

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Faculty:		Dr. Boluyt (top row, second from left) and members of LMK
	Marvin Boluyt, Ph.D. (boluytm@umich.edu), Director
Visiting Scientist:
	Agdas Mikkor (amikkor@umich.edu)
Doctoral Student
	Hyun Seok Hwang (hwanghs@umich.edu)
Laboratory Assistant:
	Georgina Cirrincione (gcirrinc@umich.edu)
Undergraduate Students:
	Esther Baik, (estherba@umich.edu) UROP *
	Julie Brevick (jbrevick@umich.edu)
	Rhett Butler (rhettb@umich.edu)
	Mike Ghannam (mousajab@umich.edu)
	Aaron Herzog (apherzog@umich.edu)
	Aaron LaRock (arlarock@umich.edu) UROP *
	Jiha Lee (jihalee@umich.edu) UROP *
	David Rogers (dsrogers@umich.edu)
	Claire Stuve (cstuve@umich.edu) UROP *
Collaborators:
	Ragavendra Baliga, M.D. UM Medical Center
	Kenneth M. Baker, M.D. Weiss Center, Geisinger Clinic, Danville, PA
	O.H.L. Bing, M.D. Boston VA Medical Center, Boston, MA
	Barry Bleske, Pharm.D. UM Pharmacy
	Wesley W. Brooks, M.D. Boston VA Medical Center, Boston, MA
	James Caffrey, Ph.D. Texas College of Osteopathic Medicine, Fort Worth, TX
	Robert Cody, M.D. UM Medical Center
	Chester H. Conrad, M.D. Boston VA Medical Center, Boston, MA
	David E. Dostal, Ph.D. Weiss Center, Geisinger Clinic, Danville, PA
	Thomas Eschenhagen, M.D. Universität Hamburg, GERMANY
	Lisa Larkin, Ph.D. UM Medical School
	M. Harold Laughlin, Ph.D. The University of Missouri, Department of Veterinary Sciences
	John M. Nicklas, M.D. UM Medical Center
	Peter Vaitkevicius, M.D. UM Medical Center
	Tania E. Webb, Ph.D. National Heart Lung and Blood Institute, London, UK
	Antoine Younes, Ph.D. Université d'Auvergne, FRANCE
* UROP is the UM's Undergraduate Research Opportunity Program, giving first- and second-year students the opportunity to work with research faculty in their labs.

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Dr. Boluyt and David Rogers in front of David's poster presentation, "Identification of Candidate Proteins for the Cardioprotective Effects of Exercise Training," researched by David S. Rogers, Zhao B. Li, Michael J. Randall, Antony F. Scalia, Marvin O. Boluyt, all from UM.

All kinds of life forms can be sighted in Chinatown!

Chinatown parade participant drums up interest.

David Rogers at Pacific Bell Park, home of the San Francisco Giants baseball team.

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