QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online December 22, 2004

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?

Yin and yang of retinal health

In diabetic retinopathy, the arteries in the retina weaken and leak, causing retinal ischaemia. New vessels develop to improve oxygenation but these haemorrhage easily and many patients eventually lose their eyesight. Paradoxically, endothelial cell apoptosis is increased in diabetic retinopathy, even though the endothelial survival factor VEGF is upregulated. On p. 243, Azza El-Remessy et al. suggest that the high glucose concentrations present in diabetic individuals block the pro-survival effects of VEGF by simultaneously decreasing the activity of Akt1, a kinase acting in an anti-apoptotic pathway downstream of VEGF, and increasing the activity of pro-apoptotic p38 MAP kinase. They show that apoptosis in retinal endothelial cells in vitro increases after treatment with glucose or peroxynitrite, a product of glucose-induced oxidative stress. These treatments decrease Akt1 phosphorylation through tyrosine nitration of the PI 3-kinase that phosphorylates Akt1 and increase phosphorylation of p38 MAP kinase. The authors conclude that upregulation of the Akt1 anti-apoptotic signalling pathway through blockade of tyrosine nitration could provide a way to control early diabetic retinopathy.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

Related articles in JCS:

Oxidative stress inactivates VEGF survival signaling in retinal endothelial cells via PI 3-kinase tyrosine nitration

Azza B. El-Remessy, Manuela Bartoli, Danial H. Platt, David Fulton, and Ruth B. Caldwell
JCS 2005 118: 243-252. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?