RESEARCH ARTICLE


The Effect of Hydrogen Peroxide on Sarco/Endoplasmic and Plasma Membrane Calcium ATPase Gene Expression in Cultured Human Lens Epithelial Cells



M.J Marian1, P Mukhopadhyay2, D Borchman*, 3, D Tang3, C.A Paterson3
1 Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40202, USA
2 Department of Molecular, Cellular and Craniofacial Biology, University of Louisville School of Dentistry, Louisville, KY 40202, USA
3 Department of Ophthalmology and Visual Sciences, University of Louisville School of Medicine, Louisville, KY 40202, USA


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© Marian et al.; Licensee Bentham Open

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

* Address correspondence to this author at the Department of Ophthalmology and Visual Sciences, University of Louisville School of Medicine, Louisville, KY 40202, USA; E-mail: borchman@louisville.edu


Abstract

The loss of calcium homeostasis in the lens of the eye appears to be a factor contributing to lens opacity. In the human lens, calcium homeostasis depends on the Ca2+-ATPase pumps found only in the epithelium. A plasma membrane calcium pump, PMCA2 is upregulated in human cataractous lenses. To determine if oxidation caused the plasma membrane Ca2+-ATPases (PMCA) or sarcoplasmic/endoplasmic Ca2+-ATPases (SERCA) to become upregulated, we cultured a human lens epithelial cell line, in the presence of hydrogen peroxide. We observed an increase in PMCA1, PMCA2 SERCA2b and SERCA3 mRNA levels and protein expression with increasing hydrogen peroxide concentrations and treatment times. Hydrogen peroxide caused a rise in the intracellular calcium which could be an initiating factor in the concerted upregulation of PMCA1 and SERCA3. Our data support the idea that oxidative stress could contribute to a selective rise in PMCA/SERCA expression in human cataractous lenses.