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Richard T. Mathias
Professor

Ph.D. University of California, Los Angeles, 1975

Basic Science Tower, T-6, Room 175
Stony Brook University
Stony Brook, NY, 11794-8661

Phone: (631) 444-3041
Email:

   

Research

My lab is involved in two areas of research, one on the lens and the other on the heart.

The lens project examines the transport properties of normal and certain mutant lenses. The goal is to understand the coupling of ion transport to water fluxes, which circulate through the avascular lens to form an internal micro circulatory system. We are specifically interested in how reductions in ion transport might compromise the circulation and lead to age onset central cataracts.

The heart project is to study the mechanisms regulating the transmural gradient in Na/K pump activity, and the purpose of the gradient. Our hypothesis on mechanism is: a transmural autocrine angiotensin system, that responds to load, regulates Na/K pump activity. Our hypothesis on purpose is: the pump gradient exists to establish a transmural gradient in calcium handling and contractility, with the endocardium seeing the greatest load and having the highest contractility. Our studies test these hypotheses. Moreover, the autocrine angiotensin system is involved in both electrical and structural remodeling, which occur during heart failure. A better understanding of this system would therefore allow preventative measures that could avoid the negative consequences of remodeling.

Selected Publications

Mathias References

Hall, J.E., and R.T. Mathias. The AQP0 puzzle. Biophysical J. 107(1):10-15. 2014.
Gao J., S. Sun, I.A. Potapova, I.S. Cohen, R.T. Mathias, and J.H. Kim. Autocrine A2 in the t-system of ventricular myocytes creates transmural gradients in ion transport: A mechanism to match contraction with load? Biophysical J106(11):2364-74. 2014.
Selitto, C., L. Li, J. Gao, M.L. Robinson, R.Z. Lin, R.T. Mathias, and T.W. White. AKT activation promotes PTEN hamartoma tumor syndrome-associated cataract development. J. Clinical Invest. 123(12):5401-09. 2013.
Gao, J., H. Wang, X. Sun, K. Varadaraj, L. Li, T.W. White, and R.T. Mathias. The effects of age on lens transport. IOVS. 54(12):7174-87. 2013.
Gao, J., X. Sun, L.C. Moore, T.W. White, P.R. Brink, and R.T. Mathias. The effect of size and species on lens intracellular hydrostatic pressure. IOVS. 54(1):183-92. 2013.
Candia, O.A., R.T. Mathias, and R. Gerometta. Fluid circulation determined in the isolated bovine lens. IOVS. 53(11):7087-96. 2012.
Kumari, S.S., S. Eswaramoorthy, R.T. Mathias, and K. Varadaraj. Unique and analogous functions of aquaporin 0 for fiber cell architecture and ocular lens transparency. Biochimica et Biophysica Acta. 1812:1089-97, 2011.
Gao, J., X. Sun, L.C. Moore, T.W. White, P.R. Brink, and R.T. Mathias. Lens intracellular hydrostatic pressure is generated by the circulation of sodium and modulated by gap junction coupling. J. Gen. Physiol. 137(6):507-20. 2011.
Brink, P.R., I.S. Cohen and, R.T. Mathias. Integration of stem cells into the cardiac syncytium: formation of gap junctions. In: Regenerating the Heart. Edited by I.S. Cohen and G.R. Gaudette. Springer, New York. Pp. 301-20. 2011.
Varadaraj, K., S.S. Kumari, and R.T. Mathias. Transgenic expression of AQP1 in the fiber cells of AQP0 knockout mouse: Effects on lens transparency. Exp Eye Res. 91(3):393-404, 2010.

 

 

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