June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Systemic administration of anti-TGFb neutralizing antibody retards wound healing in a mouse cornea post-alkali burn.
Author Affiliations & Notes
  • HIroki Iwanishi
    Opthalmology, Wakayama Medecal University, Wakayama City, Japan
  • Yuka Okada
    Opthalmology, Wakayama Medecal University, Wakayama City, Japan
  • Shinya Takami
    Drug Discovery Research, Astellas Pharma Inc., Tukuba, Japan
  • Yukari Koya
    Drug Discovery Research, Astellas Pharma Inc., Tukuba, Japan
  • Kengo Saba
    Drug Discovery Research, Astellas Pharma Inc., Tukuba, Japan
  • Shizuya Saika
    Opthalmology, Wakayama Medecal University, Wakayama City, Japan
  • Footnotes
    Commercial Relationships HIroki Iwanishi, None; Yuka Okada, None; Shinya Takami, None; Yukari Koya, None; Kengo Saba, None; Shizuya Saika, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 740. doi:
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      HIroki Iwanishi, Yuka Okada, Shinya Takami, Yukari Koya, Kengo Saba, Shizuya Saika; Systemic administration of anti-TGFb neutralizing antibody retards wound healing in a mouse cornea post-alkali burn.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):740.

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

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Abstract

Purpose: To examine the effects of systemic administration of anti-transforming growth factor b (TGFb) neutralizing antibody on the outcome of wound healing in a mouse cornea following alkali burn.

Methods: (1) Alkali burn was produced in one cornea of an adult C57BL/6 mouse (n = 24) under general anesthesia by topical 3 mL of 0.2N NaOH. At day 0 and 3 anti-mouse TGFb neutralizing antibody (R & D) or control antibody was administered through the tail vein. At day 6 the finding of each cornea (epithelial defect and stromal opacification) was evaluated by using a scoring system. At day 7 the mice were killed and the cornea was examined by using histology and immunohistochemistry. (2) The alkali burn was produced in adult mice (n = 12). At day 0 they received either i. v. anti-TGFb or control antibody. At day 5 the mice was sacrificed and the cornea was obtained. RNA was extracted from the sample and processed for real-time RT-PCR for mRNA of TGFb1, IL-6, MCP1, F4/80, and aSMA. Antibody concentration in serum was examined in each mouse in (1) and (2) experiments.

Results: Epithelial defect and stromal opacification were more marked in mice with anti-TGFb antibody as compared with control mice. Less appearance of both myofibroblasts (aSMA+) and macrophages (F4/80+) was observed in association with less accumulation of fibronectin in control cornea as compared with antibody-treated mice. There was no difference of the expression level of the components examined between tested and control group.

Conclusions: Systemic administration of anti-TGFb antibody retards wound healing in an alkali-burned cornea in mice.

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