May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Role Of P38 Map Kinase Cascade In Conjunctival Wound Healing In Mice Scar Model
Author Affiliations & Notes
  • O. Yamanaka
    Ophthalmology, Wakayama medical university, Wakayama, Japan
  • S. Saika
    Ophthalmology, Wakayama medical university, Wakayama, Japan
  • K. Ikeda
    Anatomy, Osaka city university, Osaka, Japan
  • S. Kim–Mitsuyama
    Phramacology and Molecular Therapeutics, Kumamoto University School of Medicine, Kumamoto, Japan
  • K.–I. Miyazaki
    Ophthalmology, Wakayama medical university, Wakayama, Japan
  • Y. Ohnishi
    Ophthalmology, Wakayama medical university, Wakayama, Japan
  • Footnotes
    Commercial Relationships  O. Yamanaka, None; S. Saika, None; K. Ikeda, None; S. Kim–Mitsuyama, None; K. Miyazaki, None; Y. Ohnishi, None.
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 48. doi:
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      O. Yamanaka, S. Saika, K. Ikeda, S. Kim–Mitsuyama, K.–I. Miyazaki, Y. Ohnishi; Role Of P38 Map Kinase Cascade In Conjunctival Wound Healing In Mice Scar Model . Invest. Ophthalmol. Vis. Sci. 2006;47(13):48.

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

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Purpose: : To evaluate anti–fibrogenic effects of suppression of p38 mitogen–activated kinase (MAPK) by adenoviral gene transfer of dominant–negative (DN) p38MAPK in a mouse model of post–injury conjuctival scarring. We reported the role of p38MAPK signal on fibrogenic reaction of cultured subconjunctival fibroblasts in vitro by using a specific inhibitor (2003, ARVO).

Methods: : A circumferential incision was made in conjunctiva in the equator by using scissors in the right eye of generally anesthized adult C57BL/6 mice (n = 75). DN–p38MAPK adenoviruses were topically applied. Efficacy of adenoviral gene transfer by this system was previously established by us. On day 2, 5, and 7, the eyes were processed for immunohistochemical examination, RNA extraction and real time RT–PCR for cytokine expression.

Results: : DN–p38MAPK treatment reduced protein expression of phospho–p38MAPK as compared with control eyes with non–functioning vector. Expression of type I collagen, connective tissue growth factor (CTGF), generation of smooth muscle actin–positive myofibroblasts and invasion of F4/80–labeled macrophages were all less in the DN–p38MAPK–adenoivirus groups as compared with control. Expression of collagen Ia2 and CTGF mRNA were both reduced by DN–p38MAPK gene introduction.

Conclusions: : Suppression of p38MAPK attenuated the post–injury conjunctival fibrogenic reaction in vivo in mice, supporting its effectiveness in preventing/treating conjunctival scarring.

Keywords: gene transfer/gene therapy • wound healing • signal transduction 

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