April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
The Role of PAI-1 and TGF-β1 for Atopic Cataract Formation
Author Affiliations & Notes
  • Kanji Hori
    Department of Ophthalmology, Juntendo Univ School of Med, Tokyo, Japan
  • Akira Matsuda
    Department of Ophthalmology, Juntendo Univ School of Med, Tokyo, Japan
  • Nobuyuki Ebihara
    Department of Ophthalmology, Juntendo Univ School of Med, Tokyo, Japan
  • Akira Murakami
    Department of Ophthalmology, Juntendo Univ School of Med, Tokyo, Japan
  • Kojiro Imai
    Ophthalmology, Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Satoshi Kawasaki
    Ophthalmology, Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Kazuhiko Mori
    Ophthalmology, Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Shigeru Kinoshita
    Ophthalmology, Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Kiyotaka Okada
    Department of Physiology, Kinki University School of Medicine, Sayama, Japan
  • Osamu Matsuo
    Department of Physiology, Kinki University School of Medicine, Sayama, Japan
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 806. doi:
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      Kanji Hori, Akira Matsuda, Nobuyuki Ebihara, Akira Murakami, Kojiro Imai, Satoshi Kawasaki, Kazuhiko Mori, Shigeru Kinoshita, Kiyotaka Okada, Osamu Matsuo; The Role of PAI-1 and TGF-β1 for Atopic Cataract Formation. Invest. Ophthalmol. Vis. Sci. 2011;52(14):806.

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

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Abstract

Purpose: : We previously showed Plasminogen Activator Inhibitor-1 (PAI-1), mRNA/protein expression in atopic cataracts. It was reported that PAI-1 expression is induced by, a profibrotic molecule, transforming growth factor (TGF)-β . Atopic cataract often accompany with abnormal transdifferentiation of lens epithelial cells (LEC) into myofibroblasts. In this study, we investigated the roles of PAI-1 for the pathogenesis of atopic cataracts with special reference to TGF-β.

Methods: : Real time PCR analysis was carried out to compare the TGF-β1 and TGF-β2 mRNA expression between the cDNA samples obtained during cataract surgeries from anterior capsules of atopic cataracts (n=7) and of senile cataracts (n=8). Immunohistochemical analysis was carried out with anti-α smooth muscle actin (SMA) and anti-PAI-1 antibodies using the anterior capsular tissues obtained from atopic cataracts during surgery. The lenses obtained from PAI-1 knockout (KO) mice and wild mice were incubated with recombinant (TGF)-β1 (50ng/ml). Cultured LEC were stimulated with TGF-β1, and PAI-1 and α-SMA expression by quantified by real time PCR.

Results: : The expression of TGF-β1 mRNA was significantly higher in the cDNA samples obtained from atopic cataracts compared to those from senile cataracts. PAI-1 immunostaining were localized around α-SMA positive myofibroblasts in fibrous tissues of atopic cataracts. The lenses obtained from PAI-1 KO mice were resistant for subcapsular cataract formation by TGF-β1 stimulation. PAI-1 and α-SMA mRNA expression was upregulated by 48hr-TGF-β1 stimulation.

Conclusions: : Our results suggested that PAI-1 and TGF-β1 synergistically play some roles for the pathophysiology of atopic cataracts.

Keywords: cataract • pathology: experimental 
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