Maria Valencik

Photo of Maria Valencik

Associate Professor

Department of School of Medicine - UNR
University of Nevada/Mail Stop 330
1664 North Virginia Street
Reno,  Nevada   89557

Office: (775) 784-1389
Lab: 784-6630

Fax: 784-1419

Building: Howard Medical Science,  Office 166

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B.A. University of California-Berkeley(1984)
Ph.D. University of California Los Angeles (1991)


We study the role of integrins, dimeric receptors for extracellular matrix, in cardiac myocytes. Integrins are interposed between the contractile machinery of the cardiac muscle and the extracellular matrix skeleton of the heart. The integrin receptors serve as mechanosensors, translating mechanical stress into chemical signals. We study this process using a novel transgenic mouse system, in which integrin expression by cardiac myocytes is turned on and off using a chemical switch (Transgenic Research 10: 269-75). Using a similar approach, we are studying the role of the natriuretic peptide system in mediating diastolic left ventricular function. These projects are ideal for students wishing to learn more about the basic pathobiology of the heart using molecular, cell, transgenic and physiological approaches.


Departmental Honors and University Distinction from University of California, Berkeley 1984



Older Publications

Valencik ML, and McDonald JA. Cardiac expression of a gain-of-function alpha(5)-integrin results in perinatal lethality. Am. J. Physiol. Heart Circ. Physiol. 280H, 361-7, (2001).

Keller RS, Shai SY, Babbitt CJ, Pham CG, Solaro RJ, Valencik ML, Loftus JC and Ross RS. Disruption of integrin function in the murine myocardium leads to perinatal lethality, fibrosis and abnormal cardiac performance. Am. J. Pathol. 158, 1079-90 (2001).

Valencik ML, and McDonald JA. Codon optimization markedly improves doxycycline regulated gene expression in the mouse heart. Transgenic Res. 10, 269-75 (2001).

Valencik ML, Keller RS, Loftus JC, and McDonald JA. A lethal perinatal cardiac phenotype resulting from altered integrin function in cardiomyocytes. J. Card. Fail. 84, 262-72 (2002).

Russell, L.K., C.M. Mansfield, J.J. Lehman, A. Kovacs, M. Courtois, J.E. Saffitz, M.L. Valencik, J.A. McDonald, and D. P. Kelley. Cardiac-specific induction of the transcriptional coactivator PGC-1a promotes mitochondrial biogenesis and reversible cardiomyopathy in a developmental stage-dependent manner. Circ Res. 2004 Mar 5;94(4):525-33.

Suarez, J., B. Gloss, D.D. Belke, Y. Hu, B. Scott, T. Dieterle, Y. Kim, M.L. Valencik, J.A. McDonald and W.H. Dillmann. Doxycycline inducible expression of SERCA2a improves calcium handling and reverts cardiac dysfunction in pressure overload-induced cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2004 Jul 15.