THOMAS J. EDDINGER
Professor

B.S. 1980, Purdue University
Ph.D., 1984, University of Wisconsin-Madison
Postdoctoral Fellow, University of Wisconsin Medical School and University of Virginia Medical School

WLS B06
(414) 288-1483
email: thomas.eddinger@marquette.edu

Molecular Mechanisms of Smooth Muscle Function

Muscle cells are unique in their ability to generate large amounts of force in a short period of time. In skeletal, cardiac and smooth muscle cells the method by which force is generated, the time scale required, and the mechanism for regulation are similar but yet unique. The differences within and between these tissues allow them to maximally perform their required functions.

One of the many differences between the muscle types are the contractile proteins themselves--the proteins directly involved in force generation. The major contractile proteins, actin and myosin, show tissue-specific types. These isoforms allow optimization of each muscle type for its specific function, including variation in speed of shortening, amount of force generated, and energy consumption. Differences in numerous other proteins within these cells, as well as their anatomical organization, regulatory mechanisms, innervation, etc., all contribute to the diversity between these tissues.

Research work in this lab involves the study of contractile protein isoforms in muscle including their expression, regulation and function in SM contraction. Molecular, mechanical, biochemical, histochemical, and immunological approaches are used to further our understanding of the function and regulation of these isoforms.

Recent Publications:

Govindaraju, S.R., J.L. Bain, T.J. Eddinger, D.A. Riley. 2008. Vibration causes acute vascular injury in a two-step process: vasoconstriction and vacuole disruption. Anat. Rec. (Hoboken). 291: 999-1006.

Eddinger, T.J., D.P. Meer, A.S. Miner, J.T. Meehl, A.S. Rovner, and P.H. Ratz.  2007.  Potent inhibition of Arterial smooth muscle tonic contractions by the selective myosin II inhibitor, Blebbistatin,  J. Pharmacol. Exp. Ther. 2007 320: 865-870.

Eddinger, T.J.  and D.P. Meer. 2007. Myosin II Isoforms in Smooth Muscle: Heterogeneity and Function. Am J Physiol Cell Physiol., 293: C493-C508.

Rondelli CM, Szasz IT, Kayal A, Thakali K, Watson RE, Rowner AS, Eddinger TJ, Fink GD, and Watts SW. 2007. Preferential Myosin Heavy Chain Isoform B Expression May Contribute to the Faster Velocity of Contraction in Veins Versus Arteries. J Vasc Res 44: 264-272.

Eddinger, T.J., J.D. Schiebout and D.R. Swartz. 2007.  Adherens junction associated protein distribution differs in smooth muscle tissue and acutely isolated cells. Am. J. Phys. Gastro. Liver Physiol., 292: G684-G697.

Han, S., J.E. Speich, T.J. Eddinger, K.M. Berg, A.S. Miner, C. Call, and P.H. Ratz. 2006. Evidence for absence of latchbridge formation in muscular saphenous artery. Am. J. Physiol. Heart Circ. Physiol., 291:H138-H146.

Call, C., S. Han, J.E. Speich, T.J. Eddinger, and P.H. Ratz. 2006. Role of latchbridge formation in pressurized elastic artery. Am. J. Physiol. Heart Circ. Physiol., 291: H1513- H1520 .

Recent Papers Presented at Meetings:

Isolated smooth muscle cells have different adherens junction associated protein distribution from intact tissue. Biophysical Society Meeting.  Salt Lake City, UT, February 18-22, 2006.  (Presented by T.J. Eddinger)

Recent Invited Talks:

Myosin II Isoforms in Smooth Muscle: Heterogeneity and Function. Department of Biology,
University of Wisconsin-Whitewater