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Cellular osmolytes reduce lens epithelial cell death and alleviate cataract formation in galactosemic rats.

Cellular osmolytes reduce lens epithelial cell death and alleviate cataract formation in... Many cataractogenic stresses also induce endoplasmic reticulum (ER) stress in lens epithelial cells (LECs), which appears to be one of the universal inducers of cell death. In galactosemic rats, activation of ER stress results in the activation of the unfolded protein response (UPR)-dependent death pathway, production of reactive oxygen species (ROS), and cell death. All are induced and precede cataract formation. Cellular osmolytes such as 4-phenylbutyric acid (PBA), trimethylamine N-oxide (TMAO), and tauroursodeoxychoric acid (TUDCA) are known to suppress the induction of ER stress. We investigated whether these small molecules prevent cataract formation in galactose-fed rat lenses. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular vision Pubmed

Cellular osmolytes reduce lens epithelial cell death and alleviate cataract formation in galactosemic rats.

Molecular vision , Volume 13: 9 – Sep 20, 2007

Cellular osmolytes reduce lens epithelial cell death and alleviate cataract formation in galactosemic rats.


Abstract

Many cataractogenic stresses also induce endoplasmic reticulum (ER) stress in lens epithelial cells (LECs), which appears to be one of the universal inducers of cell death. In galactosemic rats, activation of ER stress results in the activation of the unfolded protein response (UPR)-dependent death pathway, production of reactive oxygen species (ROS), and cell death. All are induced and precede cataract formation. Cellular osmolytes such as 4-phenylbutyric acid (PBA), trimethylamine N-oxide (TMAO), and tauroursodeoxychoric acid (TUDCA) are known to suppress the induction of ER stress. We investigated whether these small molecules prevent cataract formation in galactose-fed rat lenses.

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pmid
17768385

Abstract

Many cataractogenic stresses also induce endoplasmic reticulum (ER) stress in lens epithelial cells (LECs), which appears to be one of the universal inducers of cell death. In galactosemic rats, activation of ER stress results in the activation of the unfolded protein response (UPR)-dependent death pathway, production of reactive oxygen species (ROS), and cell death. All are induced and precede cataract formation. Cellular osmolytes such as 4-phenylbutyric acid (PBA), trimethylamine N-oxide (TMAO), and tauroursodeoxychoric acid (TUDCA) are known to suppress the induction of ER stress. We investigated whether these small molecules prevent cataract formation in galactose-fed rat lenses.

Journal

Molecular visionPubmed

Published: Sep 20, 2007

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