Research Paper Volume 13, Issue 13 pp 17568—17591

Aging-dependent loss of GAP junction proteins Cx46 and Cx50 in the fiber cells of human and mouse lenses accounts for the diminished coupling conductance

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Figure 5. Age-dependent changes of Cx46 and Cx50 in normal human lens fiber cells of different age groups as determined by regular western blot analysis. (A) Western blot results of Cx46 and Cx50 in human lens fibers of different age groups. Note that in 20 μg of total proteins, Cx46 and Cx50 are abundantly expressed in the 7M human lens but become barely detectable in human lenses aged 54 and older. α-Actinin was showed as a loading control. (B) Quantification results show age-dependent changes of Cx46 and Cx50 in the fiber cells of different age groups as determined in (A). (C) Western blot results of Cx46 and Cx50 in human lens fibers of different age groups. Note that in 150 μg of total proteins, Cx46 is intact with relatively strong signal in human lenses of aged 65 or younger. Cx50 appears as degraded protein. Both Cx46 and Cx50 become undetectable after 60s. α-Actinin was showed as a loading control. (D) Quantification results show age-dependent changes of Cx46 and Cx50 in the fiber cells of different age groups as determined in (C).