IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1167/iovs.08-2599 on November 7, 2008
 (Investigative Ophthalmology and Visual Science. 2009;50:1271-1282.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-2599
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
iovs.08-2599v1
50/3/1271    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Akoyev, V.
Right arrow Articles by Takemoto, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Akoyev, V.
Right arrow Articles by Takemoto, D. J.

Hypoxia-Regulated Activity of PKC{epsilon} in the Lens

Vladimir Akoyev, Satyabrata Das, Snehalata Jena, Laura Grauer, and Dolores J. Takemoto

From the Department of Biochemistry, Kansas State University, Manhattan, Kansas.

PURPOSE. To show that hypoxia is necessary to prevent opacification of the lens. Protein kinase C (PKC)-{epsilon} serves a role that is distinct from PKC-{gamma} when both PKC isoforms are expressed in the lens. PKC{epsilon} serves a very important role in hypoxic conditions, helping to prevent opacification of the lens.

METHODS. Digital image analysis, confocal microscopy, dye transfer assay, coimmunoprecipitation, Western blot analysis, and enzyme activity assays were used, respectively, to study opacification of the lens, intercellular communications, cellular localization of connexin-43 (Cx43), and the interactions between PKC{epsilon}, PKC{gamma}, and Cx43 in the lens epithelial cells.

RESULTS. Hypoxic conditions (1%–5% of oxygen) were very important in maintaining clarity of the lenses of wild-type (WT) mice. Normoxic conditions induced opacification of the WT lens. Lenses from the PKC{epsilon}-knockout mice underwent rapid opacification, even in hypoxic conditions. Hypoxia did not induce apoptosis in the lens epithelial cells, judging by the absence of active caspase-3, and it did not change intercellular communication and did not affect the number and localization of junctional Cx43 plaques in the lens epithelial cell culture. Hypoxia activated PKC{epsilon}, whereas phorbol ester (TPA), oxidation (H2O2), and insulin-like growth factor-1 (IGF-1) activated PKC{gamma} and decreased the activity of PKC{epsilon}. Hypoxia did not induce the phosphorylation of the Cx43.

CONCLUSIONS. Hypoxia-induced activation of PKC{epsilon} is very important in surviving hypoxia and maintaining the clarity of the lens. However, PKC{gamma} is utilized in the control of Cx43 gap junctions.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the Association for Research in Vision and Ophthalmology