Am J Physiol Cell Physiol AJP: Regulatory, Integrative and Comparative Physiology
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Am J Physiol Cell Physiol (January 9, 2008). doi:10.1152/ajpcell.00540.2007
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Submitted on November 14, 2007
Accepted on January 7, 2008

TAT-mediated PRDX6 protein transduction protects against eye lens epithelial cell death and delays lens opacity

Eri Kubo1, Nigar Fatma2, Yoshio Akagi1, David R Beier3, Sanjay P Singh4, and Dhirendra P Singh2*

1 Ophthalmology, University of Fukui, Fukui, Japan
2 Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, Nebraska, United States
3 Genetics, Harvard Medical School, Boston, Massachusetts, United States
4 Neurological Sciences, University of Nebraska Medical Center, Omaha, Nebraska, United States

* To whom correspondence should be addressed. E-mail: dpsingh{at}unmc.edu.

A diminished level of endogenous antioxidant in cells/tissues is associated with reduced resistance to oxidative stress. PRDX6, a protective molecule, regulates gene expression/function by controlling reactive oxygen species (ROS) levels. Using PRDX6 protein linked to TAT, the transduction domain from HIV-1 TAT protein, we demonstrated that PRDX6 was transduced into lens epithelial cells derived from rat or mouse lenses. The protein was biologically active, negatively regulating apoptosis and delaying progression of cataractogenesis by attenuating deleterious signaling. Lens epithelial cells (LECs) from cataractous lenses bore elevated levels of ROS, were susceptible to oxidative stress. These cells harbored increased levels of active TGF{beta}1, and {alpha}-SM-actin and {beta}ig-h3, markers for cataractogenesis. Importantly, cataractous lenses showed a 10-fold reduction in PRDX6 expression, while TGF{beta}1 mRNA and protein levels were elevated. The changes were reversed and cataractogenesis was delayed when PRDX6 was supplied. Results suggest that delivery of PRDX6 can postpone cataractogenesis, and this should be an effective approach to delaying cataracts and other degenerative diseases that are associated with increased ROS.




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