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PKCγ, role in lens differentiation and gap junction coupling
Satyabrata Das1, Huan Wang, Samuel A Molina
1Department of Biochemistry, Kansas State University, Manhattan, Kansas 66506, USA.
Current Eye Research
|May 24, 2011
Summary
Protein kinase C gamma (PKCγ) significantly regulates gap junction coupling in the eye lens. Its absence in knockout mice increases Cx43 expression and enhances cell-to-cell communication in lens fibers.
Area of Science:
- Ophthalmology
- Cell Biology
- Physiology
Background:
- Gap junction coupling is crucial for lens transparency and function.
- Protein kinase C gamma (PKCγ) is a potential regulator of lens gap junctions.
Purpose of the Study:
- To investigate the role of PKCγ in regulating gap junction coupling within the normal lens.
- To compare gap junction properties in wild type (WT) and PKC-γ knockout (KO) mouse lenses.
Main Methods:
- Utilized Western blotting, confocal microscopy, immunoprecipitation, and RT-PCR to assess gap junction protein and message expression.
- Measured gap junction coupling conductance and pH gating in intact lenses via impedance studies.
Main Results:
- No significant differences in lens size, clarity, or Cx46/Cx50 expression between WT and KO mice.
- PKCγ knockout lenses showed a ~150% increase in total Cx43 protein expression, with Cx43 extending into fiber cells.
- Gap junction coupling conductance increased by 34% in differentiating fibers and 82% in mature fibers of KO lenses compared to WT.
Conclusions:
- PKCγ plays a critical role in regulating gap junction expression and coupling in the normal lens.
- The absence of PKCγ leads to altered Cx43 distribution and significantly enhanced gap junction communication in the lens.
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