title: Crosstalk between TGF-beta and MAPK signaling during corneal wound healing.
abstract: OBJECTIVE
  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-β signaling plays during the healing process. To achieve this goal, they used transgenic mice in which the TGF-β 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-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.
authors.affiliation: Department of Ophthalmology, University of Cincinnati, Cincinnati, Ohio 45267-0838, USA.
authors.forename: Kazuto
authors.initials: K
authors.lastname: Terai
authors.forename: Mindy K
authors.initials: MK
authors.lastname: Call
authors.forename: Hongshan
authors.initials: H
authors.lastname: Liu
authors.forename: Shizuya
authors.initials: S
authors.lastname: Saika
authors.forename: Chia-Yang
authors.initials: CY
authors.lastname: Liu
authors.forename: Yasuhito
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Tai-ichiro
authors.initials: T
authors.lastname: Chikama
authors.forename: Jianhua
authors.initials: J
authors.lastname: Zhang
authors.forename: Noriko
authors.initials: N
authors.lastname: Terai
authors.forename: Candace W-C
authors.initials: CW
authors.lastname: Kao
authors.forename: Winston W-Y
authors.initials: WW
authors.lastname: Kao
mesh_terms: D051698:Activating Transcription Factor 2 / Q000378:metabolism; D000818:Animals; D002450:Cell Communication / Q000502:physiology*; D002465:Cell Movement; D049109:Cell Proliferation; D003646:Debridement; D019573:Epithelium, Corneal / Q000293:injuries / Q000502:physiology*; D005131:Eye Injuries / Q000378:metabolism* / Q000473:pathology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D020935:MAP Kinase Signaling System / Q000502:physiology*; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D010766:Phosphorylation; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D014945:Wound Healing / Q000502:physiology*; D014949:Wounds, Nonpenetrating / Q000378:metabolism / Q000473:pathology; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D051698:Activating Transcription Factor 2; C497106:Atf2 protein, mouse; D016212:Transforming Growth Factor beta; D048051:p38 Mitogen-Activated Protein Kinases