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Crosstalk between TGF-beta and MAPK signaling during corneal wound healing.

Authors
  • Terai, Kazuto
  • Call, Mindy K
  • Liu, Hongshan
  • Saika, Shizuya
  • Liu, Chia-Yang
  • Hayashi, Yasuhito
  • Chikama, Tai-ichiro
  • Zhang, Jianhua
  • Terai, Noriko
  • Kao, Candace W-C
  • Kao, Winston W-Y
Type
Published Article
Journal
Investigative Ophthalmology & Visual Science
Publisher
Association for Research in Vision and Ophthalmology (ARVO)
Publication Date
Oct 01, 2011
Volume
52
Issue
11
Pages
8208–8215
Identifiers
DOI: 10.1167/iovs.11-8017
PMID: 21917935
Source
Medline
License
Unknown

Abstract

The authors showed that in the absence of TGF-β 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-β 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-β and MAPK signaling pathways in corneal epithelial wound healing.

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