CCN6 as a profibrotic mediator that stimulates the proliferation of lung fibroblasts via the integrin .BETA.1/focal adhesion kinase pathway

• Batmunkh Rentsenkhand

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Nishioka Yasuhiko

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Aono Yoshinori

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Azuma Momoyo

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Kinoshita Katsuhiro

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Kishi Jun

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Makino Hideki

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Kishi Masami

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Takezaki Akio

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

• Sone Saburo

  Department of Respiratory Medicine and Rheumatology, the University of Tokushima Graduate School

Bibliographic Information

Other Title

• CCN6 as a profibrotic mediator that stimulates the proliferation of lung fibroblasts via the integrin β1/focal adhesion kinase pathway

Abstract

Idiopathic pulmonary fibrosis is a progressive and lethal disease of the lung that is characterized by the proliferation of fibroblasts and increased deposition of the extracellular matrix. The CCN6/WISP-3 is a member of the CCN family of matricellular proteins, which consists of six members that are involved in many vital biological functions. However, the regulation of lung fibroblasts mediated by CCN6 protein has not been fully elucidated. Here, we demonstrated that CCN6 induced the proliferation of lung fibroblasts by binding to integrin β1, leading to the phosphorylation of FAK^Y397. Furthermore, CCN6 showed a weak, but significant, ability to stimulate the expression of fibronectin. CCN6 was highly expressed in the lung tissues of mice treated with bleomycin. Our results suggest that CCN6 plays a role in the fibrogenesis of the lungs mainly by stimulating the growth of lung fibroblasts and is a potential target for the treatment of pulmonary fibrosis. J. Med. Invest. 58: 188-196, August, 2011

Journal

• The Journal of Medical Investigation

  The Journal of Medical Investigation 58 (3,4), 188-196, 2011

  The University of Tokushima Faculty of Medicine

Keywords

• CCN
• integrin
• proliferation
• fibroblasts
• focal adhesion kinas

Details

• CRID: 1390282679221716224
• NII Article ID: 130004822656
• NII Book ID: AA11166929
• DOI: 10.2152/jmi.58.188
• ISSN: 13496867
• ISSN: 13431420
• Web Site: http://www.jstage.jst.go.jp/article/jmi/58/3,4/58_3,4_188/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2012323183
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed