PRDX6 attenuates oxidative stress- and TGFbeta-induced abnormalities of human trabecular meshwork cells.

Published

Journal Article

Oxidative stress and TGFbeta-induced disturbance of cells and tissues are implicated in initiation and progression of pathophysiology of cells/tissues. Using primary human trabecular meshwork (TM) cells from normal and glaucomatous subjects, this study demonstrated that peroxiredoxin (PRDX) 6, an antioxidant, offsets the deleterious effects of oxidative stress on TM cells by optimizing ROS and TGFbeta levels. An analysis of glaucomatous TM cells revealed a reduced expression of PRDX6 mRNA and protein. Biochemical assays disclosed enhanced levels of ROS, as well as high levels of TGFbetas and these cells expressed elevated extracellular matrix (ECM) and Tsp1 proteins with reduced MMP2; conditions implicated in the pathophysiology of glaucoma. Non-glaucomatous TM cells exposed to TGFbetas/ROS showed similar features as in glaucomatous cells. The abnormalities induced were reversed by delivery of PRDX6. The data provide evidence that oxidative stress-induced abnormality in TM may be related to reduced PRDX6 expression and provide a foundation for antioxidant-based therapeutics for treating glaucoma.

Full Text

Duke Authors

Cited Authors

  • Fatma, N; Kubo, E; Toris, CB; Stamer, WD; Camras, CB; Singh, DP

Published Date

  • September 2009

Published In

Volume / Issue

  • 43 / 9

Start / End Page

  • 783 - 795

PubMed ID

  • 19572226

Pubmed Central ID

  • 19572226

Electronic International Standard Serial Number (EISSN)

  • 1029-2470

Digital Object Identifier (DOI)

  • 10.1080/10715760903062887

Language

  • eng

Conference Location

  • England