Biography

Dr. Wacker joined the Department of Basic Medical Science in the School of Medicine in 2007. He currently teaches physiology in the Human Structure Function series taught to the medical school students, as well as physiology courses in the Anesthesiologist Assistant program and the Physician Assistant program.

Dr. Wacker is a member of the Muscle Biology Group at UMKC with expertise in cardiac muscle physiology. The interests in his laboratory focus on agents that alter cardiac muscle function and calcium homeostasis in cardiac myocytes. Acutely, changes in calcium homeostasis can lead to arrhythmias and alteration of cardiac muscle contractility. More chronic alterations in calcium, however, can lead to remodeling of the heart as observed in cardiac hypertrophy and heart failure. Specifically, Dr. Wacker is interested in endocrine/paracrine agents which may directly alter calcium changes in cardiac myocytes via signaling mediated by membrane receptors.

Recently, Dr. Wacker and the Muscle Biology Group have worked in collaboration with the UMKC Bone Biology Group on a NIH-funded project exploring mechanisms of bone-muscle crosstalk. Dr. Wacker’s laboratory has concentrated on a hormone, FGF23, released by bone cells that may play a role in directly altering cardiac function during chronic kidney disease. Additional interests in the laboratory focus on how thromboxane A2, intracellular phosphoinositide signaling, and fibrate drugs may directly alter cardiac muscle function.

What excites you about your work?

I enjoy the problem solving and the challenge of trying to understand the mechanisms behind human health and disease. You are trying to figure out something that is unknown and has never been put in any textbook. I also enjoy mentoring students in research and watching their interest and excitement grow.

What led you to focus on research?

As an undergraduate, a gifted genetics professor involved me in research on the effects of space radiation on mutation rates in worms sent up on the space shuttle. The same semester I also served as a biology teaching assistant. Having discovered an interest in both research and teaching, I decided to pursue my Ph.D. I was passionate about physiology, so my graduate work started with a neurophysiology research project with another great mentor. We discovered that the agent we were looking at also induced abnormal heartbeats. That turned my interest toward cardiovascular physiology. Now I am investigating the interaction between heart disease and kidney disease.

What do you enjoy outside of work time?

Besides spending time with family and friends, I play softball and basketball and enjoy hitting the golf course. I also coach a youth basketball team and have been known to play on a UMKC intramural team or two. I always joked that I got into academia to prolong my intramural sports career. I just didn't know it would be this long.

Research Focus

Exploring the mechanisms for cardiovascular disease suffered by kidney disease patients.

Most patients with kidney disease actually die of cardiovascular disease, Wacker says, so his lab is trying to figure out which chemical agents in kidney disease patients could be affecting cardiac muscle or blood vessel function in ways that can lead to heart disease.

Research Summary

My laboratory is interested in agents that alter cardiac muscle function and calcium homeostasis in cardiac myocytes. I am specifically interested in endocrine/paracrine agents which may directly alter cardiac function. One main area of focus currently in the lab is on hormones/toxins (e.g. FGF23) that are elevated during chronic kidney disease that may cause heart disease. Typical experiments in the lab center around measuring cardiac contractility/ function, Langendorf perfusion of isolated hearts, calcium imaging of cardiac myocytes, cardiac gene/protein changes, exploring cardiac myocyte signal transduction mechanisms like IP3 signaling, and blood vessel function.

Selected Publications

Avin KG, Vallejo JA, Chen NX, Wang K, Touchberry CD, Brotto M, Dallas SL, Moe SM, Wacker MJ. Fibroblast Growth Factor 23 does not directly influence skeletal muscle cell

proliferation and differentiation or ex vivo muscle contractility. American Journal of Physiology: Endocrinology and Metabolism. 315 (4): E594-E604. 2018. PMID: 29558205.

Grabner A, Schramm K, Silswal N, Hendrix M, Yanucil C, Czaya B, Singh S, Wolf M, Hermann S, Stypmann J, Di Marco G, Brand M, Wacker MJ, and Faul C. FGF23/FGFR4-mediated left ventricular hypertrophy is reversible. Scientific Reports. 7 (1):1993. 2017.

Wacker MJ, Touchberry CD, Silswal N, Brotto L, Elmore CJ, Bonewald LF, Andresen J, Brotto M. Skeletal muscle, but not cardiovascular function, is altered in a mouse model of autosomal recessive hypophosphatemic rickets. Frontiers in Physiology. 7:173. 2016.

Silswal N, Parelkar N, Andresen J, Wacker MJ. Restoration of endothelial function in Ppara^-/- mice by tempol. PPAR Research. Article ID 728494, 2015.

Touchberry CD, Silswal N, Tchikrizov V, Elmore CJ, Srinivas S, Akthar AS, Swan HK, Wetmore LA, Wacker MJ. Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB. BMC: Pharmacology and Toxicology. 15: 73, 2014.

Silswal N, Touchberry CD, Daniel DR, McCarthy DL, Zhang S, Andresen J, Stubbs JR, Wacker MJ. FGF23 directly impairs endothelium-dependent vasorelaxation by increasing superoxide levels and reducing nitric oxide bioavailability. American Journal of Physiology: Endocrinology and Metabolism. 307 (5): E426-36, 2014.

Gallagher PM, Touchberry CD, Teson K, McCabe E, Tehel M, Wacker MJ. Effects of an acute bout of resistance exercise on fiber-type specific GLUT4 and IGF-1R expression. Applied Physiology, Nutrition, and Metabolism. 38 (5): 581-586, 2013.

Touchberry CD, Green TM, Tchikrizov V, Mannix JE, Mao TF, Carney BW, Girgis M, Vincent RJ, Wetmore LA, Dawn B, Bonewald L, Stubbs JR, Wacker MJ. FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy. American Journal of Physiology: Endocrinology and Metabolism. 304 (8): E863-73, 2013.

Bonewald LF, Wacker MJ. FGF23 Production by Osteocytes. Pediatric Nephrology. 28 (4): 563-568. 2013.