AI Article Synopsis
- The study investigates how gap junction channels, made of alpha3 (Cx46) and alpha8 (Cx50) connexin subunits, contribute to lens development and transparency in the eye.
- Researchers created double knockout mice (alpha3(-/-) alpha8(-/-)) to analyze the effects of missing these gap junctions on lens health.
- The findings revealed that without these channels, the lenses developed severe cataracts and lost significant levels of gamma-crystallin proteins, highlighting the critical role of gap junctions in maintaining lens cell stability and function.
Article Abstract
Lens development and transparency have been hypothesized to depend on intercellular gap junction channels, consisting of alpha3 (Cx46) and alpha8 (Cx50) connexin subunits, to transport metabolites, secondary messages and ions between lens cells. To evaluate this hypothesis, we have generated alpha3(-/-) alpha8(-/-) double knockout mice and characterized their lens phenotypes. Without gap junctions between lens fiber cells, alpha3(-/-) alpha8(-/-) lenses displayed severe cataracts resulting from cell swelling and degeneration of inner fibers while normal peripheral fiber cells continued to form throughout life. Neither an increase of degraded crystallins nor an increase of water-insoluble crystallins was found in alpha3(-/-) alpha8(-/-) lenses. However, a substantial reduction of gamma-crystallin proteins, but not alpha- and beta-crystallins, was detected. These results suggest that gap junction communication is important for maintaining lens homeostasis of inner fiber cells and that a loss of gap junctions leads to cataract formation as well as reductions of gamma-crystallin proteins and transcripts.
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| http://dx.doi.org/10.1016/j.exer.2006.03.013 | DOI Listing |
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