Richard T. Mathias

FACULTY


Richard T. Mathias 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: Richard.Mathias@stonybrook.edu

Research

HEART

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.

LENS

The lens project focuses on the circulation of salt and water therough and around the lens.  Our hypothesis is that spatially separate ion transport systems generate a circulation of salt, which through osmosis, generate a circulation of fluid.  The circulation of fluid provides an internal micro circulatory system for the avascular lens. This system brings nutrients and anti-oxidants to central fiber cells and carries waste products to surface epithelial cells where they can be broken down or eliminated.  Associated with the circulation of salt, there are internal spatial gradients in ion concentrations and voltage, whereas associated with the circulation of fluid, their internal gradients in hydrostatic pressure.  The micro circulatory system is essential for homeostasis of central fiber cells and its compromise through age and oxidation appears to be a major factor in age related cataracts. Moreover, active maintenance of the circulation is necessary for other optical properties of the lens.

Selected Publications


Mathias References
Kumari, S., Gao, J., Mathias, R.T., Sun, X, Eswaramororthy, A., Browne, N., Zhang, N., Varadaraj, K. Aquaporin 0 modulates lens gap junctions in the presence of lens-specific beaded filament proteins. Invest Ophthalmol Vis Sci.58(14):6006-6019. 2017. 
Minoque, P.J., Gao, J., Zoltoski, R.K., Novak, L.A., Mathias, R.T., Beyer, E.C., Berthoud, V.M. Physiological and optical alterations precede the appearance of cataracts in Cx46fs380 mice.  Invest Ophthalmol Vis Sci. 58(10):4366-4374. 2017.
Kim, J.H. Jiang, Y.P, Cohen, I.S., Lin, R.Z., Mathias, R.T. Pressure-overload-induced angiotensin-mediated early remodeling in mouse heart.  PLoS One. 12(5):e0176713. 2017
Cohen, I.S., Mathias, R.T. The renin-angiotensin system regulates transmural electrical remodeling in response to mechanical load. Prog  Biophys Mol Biol. 122(3):187-201. 2016
Gao, J., Sun, X., White, T.W., Delamere, N.A., Mathias, R.T. Feedback regulation of intracellular hydrostatic pressure in surface cells of the lens. Biophys J. 109(9):1830-9. 2015
Kim, J.H., Gao, J., Cohen, I.S., Mathias, R.T. Angiotensin II Type 1 receptor-mediated electrical remodeling in mouse cardiac myocytes. PLoS One. 10(10):e018711. 2015
Kumari, S., Gupta, N., Shiels, A., Fitzgerald, P.G., Menon, A.G., Mathias, R.T., Varadaraj, K. Role of aquaporin 0 in lens biomechanics. Biochem. Biophy. Res. Commun. 462(4): 339-45. 2015
Cheng, C., Nowak, R., Gao, J., Sun, X., Lo, W.K., Mathias, R.T., Fowler, V. Lens ion  homeostasis relies on the assembly of large connexin 46 gap junction plaques on the broad sides of differentiating fiber cells. Am. J. Physiol. 308(10):C835-47. 1015