Wacker Research Lab

Michael Wacker, Ph.D., now an associate professor, joined the Department of Basic Medical Science in the School of Medicine in 2007 with an adjunct appointment in the School of Nursing and Health Studies. He currently teaches physiology in the human structure function series as well as for the Anesthesiologist Assistant and Physician Assistant programs. Wacker’s research expertise is in cardiovascular physiology, which complements the research of the MUBIG team. His laboratory primarily focuses on agents that alter cardiac muscle function, disrupt calcium homeostasis in cardiac myocytes and impair vascular relaxation. Understanding these mechanisms is critical for identifying the cause of arrhythmias, pathological cardiac hypertrophy and heart failure, and ultimately in developing novel treatments for cardiovascular disease (CVD).

Picture of research from Wacker LabOne specific area of research emphasis has been on endocrine and paracrine agents that are elevated during chronic kidney disease (CKD) that may promote CVD. CVD is the major cause of mortality in the CKD population, so finding the link between these two diseases is critical to understanding and identifying treatments for both CKD and CVD. One factor, FGF23, has been shown to be released by bone cells in high amounts during CKD and may play a direct role in altering cardiovascular function. Thus, bone/kidney/heart crosstalk has become an important area of exploration for Wacker’s laboratory including collaborations with members of the Bone Biology Group at UMKC and The Kidney Institute at KU Medical Center in investigating this exciting new area of research.

Another research interest in the laboratory includes investigating the inflammatory agent thromboxane A2. Thromboxane may promote arrhythmias and cell death via direct actions on cardiac myocytes when it is released during heart attacks or during inflammatory responses. Additional research projects in the lab have investigated the effects of phosphoinositide signaling and fibrate drugs on cardiac and vascular function.

Funding

  • American Heart Association Scientist Development Grant (RC2AR058962) (PI)
  • NIH NIAMS Grand Opportunities Grant (11SDG5330016) (Co-I; PI Bonewald)
  • NIH NIA Program Project Grant 1P01AG039355-01A1 (Co-Director; PI Bonewald)
  • American Heart Association Post-Doctoral Fellowship (Silswal) (Co-Mentor with Andresen)
  • Missouri Life Science Research Board/Center for Mineralized Tissue (PI and Co-PI with Brotto)

Lab Members

  • Darla McCarthy (Associate Professor)
  • Neerupma Silswal (Post-Doctoral Fellow)
  • Sreedeepthi Bommireddipalli (Master’s student)
  • Becky Daniel (Medical student)
  • Matt Hendrix (Medical student)
  • Chelsea Shapland (Medical student)
  • Halee Patel (Medical student)
  • Tarana Gill (Medical student)
  • Sachin Nair (Medical student)
  • Fedra Fallahian (Medical student)
  • Carlee Oakley (Medical student)
  • Siri Kommareddy (Medical student)

Selected Publications

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.

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.

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

Romero-Suarez S, Mo C, Touchberry C, Lara N, Baker K, Craig R, Brotto L, Andresen J, Wacker M, Kaja S, Abreu E, Dillmann W, Mestril R, Brotto M, Nosek T. Hyperthermia: From Diagnostic and Treatments to New Discoveries. Recent Patents in Biotechnology. 6 (3): 172-183. 2012.

Touchberry CD, Elmore CJ, Nguyen TM, Andresen JJ, Zhao X, Orange M, Weisleder N, Brotto M, Claycomb WC, Wacker MJ. Store-Operated Calcium Entry is Present in HL-1 Cardiomyocytes and Contributes to Resting Calcium. Biochemical and Biophysical Research Communications. 416 (1-2): 45-50. 2011.

Touchberry CD, Bales IK, Stone JK, Rohrberg TJ, Parelkar NK, Nguyen T, Fuentes O, Liu X, Qu CK, Andresen JJ, Valdivia HH, Brotto M, Wacker MJ. Phosphatidylinositol 3,5-Bisphosphate (PI(3,5)P2) Potentiates Cardiac Contractility Via Activation of the Ryanodine Receptor. Journal of Biological Chemistry. 285 (51): 40312-21. 2010.

Romero-Suarez S, Shen J, Brotto L, Hall T, Mo CL, Valdivia HH, Andresen J, Wacker M, Nosek TM, Qu CK, Brotto M. Muscle-specific inositide phosphatase (MIP/MTMR14) is reduced with age and its loss accelerates skeletal muscle aging process by altering calcium homeostasis. Aging. 2 (8): 504-513. 2010.

Wacker MJ, Kosloski LM, Gilbert WJ, Touchberry CD, Moore DS, Kelly JK, Brotto MA, Orr JA. Inhibition of thromboxane A2 -induced arrhythmias and intracellular calcium changes in cardiac myocytes by blockade of the IP3 pathway. Journal of Pharmacology and Experimental Therapeutics. 331: 917-924, 2009.

Wacker MJ, Tehel MM, Gallagher PM. Technique for quantitative RT-PCR analysis directly from single muscle fibers. Journal of Applied Physiology 105: 308-315, 2008.