Linked Life Data

20844585

Source:http://linkedlifedata.com/resource/pubmed/id/20844585

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-9-16
pubmed:abstractText
Cataracts, named for any opacity in the ocular lens, remain the leading cause of vision loss in the world. Non-surgical methods for cataract prevention are still elusive. We have genetically tested whether enhanced lens gap junction communication, provided by increased ?3 connexin (Cx46) proteins expressed from ?8(Ki?3) knock-in alleles in Gja8tm1(Gja3)Tww mice, could prevent nuclear cataracts caused by the ?B-crystallin S11R mutation in CrygbS11R/S11R mice. Remarkably, homozygous knock-in ?8(Ki?3/Ki?3) mice fully prevented nuclear cataracts, while single knock-in ?8(Ki?3/-) allele mice showed variable suppression of nuclear opacities in CrygbS11R/S11R mutant mice. Cataract prevention was correlated with the suppression of many pathological processes, including crystallin degradation and fiber cell degeneration, as well as preservation of normal calcium levels and stable actin filaments in the lens. This work demonstrates that enhanced intercellular gap junction communication can effectively prevent or delay nuclear cataract formation and suggests that small metabolites transported through gap junction channels protect the stability of crystallin proteins and the cytoskeletal structures in the lens core. Thus, the use of an array of small molecules to promote lens homeostasis may become a feasible non-surgical approach for nuclear cataract prevention in the future.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1932-6203
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Connexin mediated cataract prevention in mice.
pubmed:affiliation
Vision Science Program and School of Optometry, University of California, Berkeley, California, United States of America.
pubmed:publicationType
Journal Article, In Vitro, Research Support, N.I.H., Extramural