| First Author | Sellitto C | Year | 2004 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 45 |
| Issue | 9 | Pages | 3196-202 |
| PubMed ID | 15326140 | Mgi Jnum | J:93048 |
| Mgi Id | MGI:3055646 | Doi | 10.1167/iovs.04-0194 |
| Citation | Sellitto C, et al. (2004) Connexin50 is essential for normal postnatal lens cell proliferation. Invest Ophthalmol Vis Sci 45(9):3196-202 |
| abstractText | PURPOSE: Connexin50 (Cx50) is absolutely essential for normal postnatal lens growth. Deletion of Cx50 or replacement with Cx46 by knockin resulted in smaller lenses containing fewer cells. To determine why Cx50-deficient lenses fail to grow normally, cell proliferation was assayed during the period of growth failure. METHODS: Wild-type, Cx50-knockout, and Cx50KI46 mice were injected with 5'-bromo-2'-deoxyuridine (BrdU) and lenses were dissected and fixed after 1 hour or 24 hours. BrdU incorporation was visualized by immunocytochemical staining, and the mitotic index (MI) was determined between postnatal day (P)0 and P6. Levels of total ERK and phospo-ERK were determined by Western blot analysis. RESULTS: On P2 to P3, wild-type lenses displayed a significantly increased MI not evident in knockout lenses, and knockin lenses only partially rescued the growth deficit. Reductions in the number of mitotic cells did not reflect a decrease in the rate of cell division and temporally correlated with reduction in lens mass. Levels of phosphorylated ERK1/2 were identical in wild-type and Cx50-deficient lens epithelia. CONCLUSIONS: These results demonstrate that Cx50-mediated communication is necessary to achieve peak mitosis. In addition, they suggest a novel mitogenic role for gap junctional coupling that is connexin specific and independent of MAPK signaling. |
