June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Loss of tenascin X suppresses expression of VEGF in macrophages and of TGFb1 in ocular fibroblasts in vitro; possible mechanism of inhibition of neovascularization in cornea
Author Affiliations & Notes
  • Takayoshi Sumioka
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Yuka Okada
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Ken-ichi Matsumoto
    Interdisciplinary Center for Science Research, Department of Biosignaling and Radioisotope Experiment, Shimane University, Shimane, Japan
  • Osamu Yamanaka
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Masayasu Miyajima
    Animal center, Wakayama Medical University, Wakayama, Japan
  • Shizuya Saika
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Footnotes
    Commercial Relationships Takayoshi Sumioka, None; Yuka Okada, None; Ken-ichi Matsumoto, None; Osamu Yamanaka, None; Masayasu Miyajima, None; Shizuya Saika, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4498. doi:
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    • Get Citation

      Takayoshi Sumioka, Yuka Okada, Ken-ichi Matsumoto, Osamu Yamanaka, Masayasu Miyajima, Shizuya Saika; Loss of tenascin X suppresses expression of VEGF in macrophages and of TGFb1 in ocular fibroblasts in vitro; possible mechanism of inhibition of neovascularization in cornea. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4498.

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

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Abstract

Purpose: To examine mRNA expression level of angiogenic growth factors, VEGF and TGFb1, in macrophages and ocular fibroblasts derived from a tenascin X-null mouse. We previously reported that the loss of tenascin X suppress neocvascularization with reduction of in vivo expression of angiogenic growth factors in a mouse cornea (ARVO 2014).

Methods: Peritoneal macrophages were obtained from tenascin X-null and wild types mice by using macrophage induction by oyster glycogen i.p. injection. Ocular fibroblasts were cultured from eye-shells of post-natal day 1 or 2 mice. The cultures were maintained for 24 hrs with or without exogenous TGFb1 and processed for RNA extraction. Real-time RT-PCR was ran to examine the expression level of VEGF and TGFb1.

Results: Loss of tenascin X supprsss mRNA expression of VEGF in macrophages and of TGFb1 in fibroblasts in the absence of TGFb1. Loss of tenascin X did not attenuate the TGFb1 induction of VEGF and TGFb1 in these cell types.

Conclusions: Tenascin X is involved in expression of angiogenic growth factors in macrophages and fibroblasts, partially explain the mechanism of inhibition of in vivo neovascularization in a tenacin X-null mouse cornea.

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