| First Author | Terai K | Year | 2011 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 52 |
| Issue | 11 | Pages | 8208-15 |
| PubMed ID | 21917935 | Mgi Jnum | J:189493 |
| Mgi Id | MGI:5445873 | Doi | 10.1167/iovs.11-8017 |
| Citation | Terai K, et al. (2011) Crosstalk between TGF-beta and MAPK signaling during corneal wound healing. Invest Ophthalmol Vis Sci 52(11):8208-15 |
| abstractText | PURPOSE: The aim of this study was to elucidate the mechanisms governing epithelial cell migration and proliferation during wound healing. METHODS: The authors used wound healing of mouse corneal epithelium to examine the role TGF-beta signaling plays during the healing process. To achieve this goal, they used transgenic mice in which the TGF-beta receptor type II (Tbr2) was conditionally ablated from the corneal epithelium. Epithelium debridement wounds were made, followed by the assessment of cell migration, proliferation, and immunostaining of various signaling pathway components. RESULTS: The authors showed that in the absence of TGF-beta signaling corneal epithelial wound healing is delayed by 48 hours; this corresponds to a delay in p38MAPK activation. Despite the delayed p38MAPK activation, ATF2, a substrate of p38MAPK, is still phosphorylated, leading to the suppression of cell proliferation at the leading edge of the wound. These data provide evidence that in the absence of TGF-beta signaling, the suppression of cell proliferation during the early stages of wound healing is maintained through the JNK activation of ATF2. CONCLUSIONS; Together the data presented here demonstrate the importance of the TGF-beta and MAPK signaling pathways in corneal epithelial wound healing. |
