Myocardin-related transcription factor A (MRTF-A) regulates TGF-β2-induced type I collagen production in human lens epithelial cells

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  • Okuno Takashi
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan
  • Imaizumi Toshiyasu
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan
  • Sakamoto Umi
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan
  • Sakai Daisuke
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan
  • Fukuda Kazuhiro
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan
  • Sanbe Atsushi
    Department of Pharmacotherapeutics, Iwate Medical University, Yahaba, Japan
  • Mayanagi Taira
    Department of Neuroscience, Institute for Biomedical Sciences, Iwate Medical University, Yahaba, Japan
  • Sobue Kenji
    Department of Neuroscience, Institute for Biomedical Sciences, Iwate Medical University, Yahaba, Japan
  • Kurosaka Daijiro
    Department of Ophthalmology, School of Medicine, Iwate Medical University, Morioka, Japan

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  • Myocardin関連転写因子A（MRTF-A）は, ヒト水晶体上皮細胞においてTGF-β2の誘導によりI型コラーゲン産生を調節する

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Abstract

We performed several experiments using human lens epithelium B3 (HLE-B3) cells to clarify whether myocardin-related transcription factor A (MRTF-A) affects type I collagen expression in transforming growth factor-β (TGF-β) -stimulated lens epithelial cells. To study the effect of MRTF-A, HLE-B3 cells were transfected with a small-interfering RNA (siRNA) against MRTF-A and cultured with or without TGF-β2. The effect of CCG203971, an MRTF-A inhibitor, onα-smooth muscle actin (α-SMA) and type I collagen expression was also examined. Gene expression was studied by quantitative real-time PCR, and subcellular localization of MRTF-A was studied by immunocytochemistry. TGF-β2 treatment promoted nuclear translocation of MRTF-A from the cytoplasm. TGF-β2 treatment increasedα-SMA and type I collagen expression in HLE-B3 cells transfected with control siRNA, but not in MRTF-A siRNA transfectants. In addition, CCG203971 abolished TGF-β2-dependentα-SMA and type I collagen induction. Our results showed that TGF-β2 promotedα-SMA and type I collagen expression in HLE-B3 cells by stimulating the nuclear translocation of MRTF-A. These findings suggest that CCG203971, as can MRTF-A inhibitor, may prevent deterioration of visual quality by anterior subcapsular cataracts and posterior capsular opacification.

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