The progression of cardiopulmonary disease and the efficacy of therapeutic interventions are critically dependent on the response of cardiac, smooth, and skeletal muscles in the cardiovascular and pulmonary systems. All three muscle types are essential for normal cardiopulmonary function, all three play key roles in cardiovascular and pulmonary disease, and all are targets for therapeutic development. The current program targets this area of biomedicine by training predoctoral and medical students for muscle research in the context of cardiopulmonary disease. The University of Kentucky (UK) is ideally suited for the program. UK is a public research institution with 33,692 undergraduate and graduate students, 1,920 faculty members, extramural research support of $290 million in 2006, and a medical center comprising six different health- related Colleges. A recently-adopted strategic plan calls for rapid growth of UK research via added faculty, expanded graduate programs, and new research facilities. Within this dynamic academic environment, the UK program for Research Training in Muscle Biology of Cardiopulmonary Disease will builds on institutional strengths to train exceptional students for careers in basic and translational research. In a highly-selective vetting process, program leadership will identify and recruit the best-qualified applicants for participation in two elite programs. Graduate students from eight different PhD programs will compete for two-year, full-time appointments in the Postdoctoral Scholar program. A similar competition will identify research-oriented medical students for an eight-week Summer Scholar program. Both groups of Scholars will be mentored by twenty-two faculty members from ten basic science and clinical departments. Multidisciplinary mentoring teams will train Scholars in relevant areas of cardiac, vascular smooth, and respiratory skeletal muscle biology. Individualized curricula will combine coursework, laboratory training, and a structured clinical experience to achieve three specific aims: 1.) To prepare basic scientists at the predoctoral level for successful long-term careers in cardiopulmonary research;2.) To engage predoctoral medical students in a summer laboratory experience that stimulates ongoing interest in basic and translational research;and 3.) To foster excellence in the mentoring skills of both program faculty and predoctoral scholars.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL086341-05
Application #
8244994
Study Section
Special Emphasis Panel (ZHL1-CSR-M (O2))
Program Officer
Tigno, Xenia
Project Start
2008-04-01
Project End
2014-03-31
Budget Start
2012-04-01
Budget End
2014-03-31
Support Year
5
Fiscal Year
2012
Total Cost
$82,367
Indirect Cost
$9,976
Name
University of Kentucky
Department
Physiology
Type
Schools of Medicine
DUNS #
939017877
City
Lexington
State
KY
Country
United States
Zip Code
40506
Waters-Banker, Christine; Butterfield, Timothy A; Dupont-Versteegden, Esther E (2014) Immunomodulatory effects of massage on nonperturbed skeletal muscle in rats. J Appl Physiol (1985) 116:164-75
Fry, Christopher S; Lee, Jonah D; Jackson, Janna R et al. (2014) Regulation of the muscle fiber microenvironment by activated satellite cells during hypertrophy. FASEB J 28:1654-65
Waters-Banker, Christine; Dupont-Versteegden, Esther E; Kitzman, Patrick H et al. (2014) Investigating the mechanisms of massage efficacy: the role of mechanical immunomodulation. J Athl Train 49:266-73
Wolff, Gretchen; Duncan, Marilyn J; Esser, Karyn A (2013) Chronic phase advance alters circadian physiological rhythms and peripheral molecular clocks. J Appl Physiol (1985) 115:373-82
Stasko, Shawn A; Hardin, Brian J; Smith, Jeffrey D et al. (2013) TNF signals via neuronal-type nitric oxide synthase and reactive oxygen species to depress specific force of skeletal muscle. J Appl Physiol (1985) 114:1629-36
Kiper, Carmen; Grimes, Barry; Van Zant, Gary et al. (2013) Mouse strain determines cardiac growth potential. PLoS One 8:e70512
Holler, Christopher J; Webb, Robin L; Laux, Ashley L et al. (2012) BACE2 expression increases in human neurodegenerative disease. Am J Pathol 180:337-50
Gilliam, Laura A A; Moylan, Jennifer S; Patterson, Elaine W et al. (2012) Doxorubicin acts via mitochondrial ROS to stimulate catabolism in C2C12 myotubes. Am J Physiol Cell Physiol 302:C195-202
Gilliam, Laura A A; Moylan, Jennifer S; Ann Callahan, Leigh et al. (2011) Doxorubicin causes diaphragm weakness in murine models of cancer chemotherapy. Muscle Nerve 43:94-102
Gilliam, Laura A A; Moylan, Jennifer S; Ferreira, Leonardo F et al. (2011) TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm weakness. Am J Physiol Lung Cell Mol Physiol 300:L225-31

Showing the most recent 10 out of 15 publications