English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Background  The purpose of this study was to address the question of how the premature senescence process may affect corneal endothelium after penetrating keratoplasty, because the quality of donor corneal endothelial cells is important for corneal transplant success.    Methods  The cell senescence and induced oxidative stress in corneal endothelium were assessed using a normal-risk orthotopic mice corneal transplantation model. Senescence associated beta-galactosidase (SA-beta-Gal) staining was used to evaluate premature senescence in the endothelium of corneal allografts. Oxidative Stress and Antioxidant Defense RT 2 -PCR Arrays and  in vitro  experimental model using H 2 O 2  treatment were used to investigate the possible mechanism.    Results  SA-beta-Gal positivity was observed obviously in mice corneal endothelium of allogenic group and the levels of p16 INK4a  message and protein increased in endothelium of allogenic group compared to syngenic group. By PCR array, an oxidant-antioxidant imbalance was found in the endothelium of corneal allograft after PKP. The results from mice model were validated using human endothelium samples of corneal allograft after PKP. We also developed an  in vitro  experimental model using H 2 O 2  treatment to simulate a state of oxidative stress in cultured human corneal endothelial cells (HCECs) and found that elevated ROS levels, the up-regulation of CDK inhibitors and ROS-mediated p16 INK4A  up-regulation in HCECs occur via the ASK1-p38 MAPK pathway.    Conclusions  Our results demonstrate the presence of oxidative stress and premature senescence in the endothelium of corneal allografts following PKP.    Electronic supplementary material  The online version of this article (doi:10.1186/s12886-016-0192-6) contains supplementary material, which is available to authorized users.

Oxidative stress and premature senescence in corneal endothelium following penetrating keratoplasty in an animal model