May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Role of p38 Map Kinase Cascade in Conjunctival Wound Healing In Vitro
Author Affiliations & Notes
  • O. Yamanaka
    Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan
  • S. Saika
    Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan
  • K. Miyazaki
    Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan
  • K. Inoue
    Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan
  • Y. Ohnishi
    Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan
  • A. Ooshima
    Department of Pathology, Wakayama Medical College, Wakayama, Japan
  • Footnotes
    Commercial Relationships  O. Yamanaka, None; S. Saika, None; K. Miyazaki, None; K. Inoue, None; Y. Ohnishi, None; A. Ooshima, None.
  • Footnotes
    Support  grant 13771037 from the Ministry of Education, Science, Sports and Culture of Japan
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1190. doi:
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    • Get Citation

      O. Yamanaka, S. Saika, K. Miyazaki, K. Inoue, Y. Ohnishi, A. Ooshima; Role of p38 Map Kinase Cascade in Conjunctival Wound Healing In Vitro . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1190.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose:To examine the role of cell signaling by p38 mitogen-activated kinase (MAPK), one of the TGF ß-stimulated signals, in cell migration, proliferation and type I collagen production in cultured human subconjunctival fibroblasts. Methods: Subconjunctival fibroblasts were obtained by outgrowth of subconjunctival tissues excised during strabismus surgery with the informed consent from each patient. Effects of a p38MAPK inihibitor (SB202190) on type I collagen production and wound closure in monolayer cell sheet were examined in confluent cultures in the presence or absence of TGFß1 at 10 ng/ml. Concentrations of collagen type I peptide in both culture medium and cell lysate in conditions above mentioned were determined using enzyme immunoassay kits. Cell proiliferation was assayed by BrdU incorporation.Results: The p38 inhibitor reduced the production of type I collagen by the fibroblasts treated by exogenous TGFß1, but had no effect on that in untreated fibroblasts. Adding the p38 inhibitor reduced the ratio of in vitro wound closure, but did not affect with the cell proliferation.Conclusions: Signaling cascade through p38MAPK has an important role in up-regulation of type I collagen accelerated by exogenous TGFß1, but has a minimal effect on basal level collagen expression. P38MAPK has also an important role in migration of cultured subconjunctival fibroblasts. These data suggest an anti-fibrotic effect of a p38MAPK inhibitor in a specialized injured site with a minimal effect on uninjured ocular surface.

Keywords: wound healing • signal transduction • conjunctiva 
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