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ID 46910
フルテキストURL
著者
Tetsunaga, Tomonori Department of Cardiovascular Physiology, Biophysiological Sciences, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Furumatsu, Takayuki Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Abe, Nobuhiro Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Nishida, Keiichiro Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Naruse, Keiji Department of Cardiovascular Physiology, Biophysiological Sciences, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Ozaki, Toshifumi Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
抄録
Biomechanical stimuli have fundamental roles in the maintenance and remodeling of ligaments including collagen gene expressions. Mechanical stretching signals are mainly transduced by cell adhesion molecules such as integrins. However, the relationships between stress-induced collagen expressions and integrin-mediated cellular behaviors are still unclear in anterior cruciate ligament cells. Here, we focused on the stretch-related responses of different cells derived from the ligament-to-bone interface and midsubstance regions of human anterior cruciate ligaments. Chondroblastic interface cells easily lost their potential to produce collagen genes in non-stretched conditions, rather than fibroblastic midsubstance cells. Uni-axial mechanical stretches increased the type I collagen gene expression of interface and midsubstance cells up to 14- and 6-fold levels of each non-stretched control, respectively. Mechanical stretches also activated the stress fiber formation by shifting the distribution of integrin αVβ3 to the peripheral edges in both interface and midsubstance cells. In addition, integrin αVβ3 colocalized with phosphorylated focal adhesion kinase in stretched cells. Functional blocking analyses using anti-integrin antibodies revealed that the stretch-activated collagen gene expressions on fibronectin were dependent on integrin αVβ3-mediated cellular adhesions in the interface and midsubstance cells. These findings suggest that the integrin αVβ3-mediated stretch signal transduction might have a key role to stimulate collagen gene expression in human anterior cruciate ligament, especially in the ligament-to-bone interface.
キーワード
Anterior cruciateligament
Collagen
Integrin αVβ3
Interface
Mechanical stretch
発行日
2009-09-18
出版物タイトル
Journal of Biomechanics
42巻
13号
出版者
Elsevier Sci Ltd.
開始ページ
2097
終了ページ
2103
ISSN
0021-9290
NCID
AA00694200
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
© 2009 Elsevier Ltd. All rights reserved.
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