TY - JOUR
T1 - Mechanical stretch increases CCN2/CTGF expression in anterior cruciate ligament-derived cells
AU - Miyake, Yoshiaki
AU - Furumatsu, Takayuki
AU - Kubota, Satoshi
AU - Kawata, Kazumi
AU - Ozaki, Toshifumi
AU - Takigawa, Masaharu
N1 - Funding Information:
We thank Ms. Motomi Hachioji, Dr. Aki Yoshida, and Dr. Eriko Aoyama for their kind cooperation. We are also grateful to Dr. Nobuhiro Abe for providing tissue samples. This work was supported by Japan Society for the Promotion of Science (Nos. 19109008 , 20791040 , and 21592360 ), JSPS Fujita Memorial Fund for Medical Research, the Japanese Foundation for Research and Promotion of Endoscopy, Okayama Medical Foundation, Japan Orthopaedics and Traumatology Foundation (No. 225), and Child Health and Development from the Ministry of Health, Labor and Welfare.
PY - 2011/6/3
Y1 - 2011/6/3
N2 - Anterior cruciate ligament (ACL)-to-bone interface serves to minimize the stress concentrations that would arise between two different tissues. Mechanical stretch plays an important role in maintaining cell-specific features by inducing CCN family 2/connective tissue growth factor (CCN2/CTGF). We previously reported that cyclic tensile strain (CTS) stimulates α1(I) collagen (COL1A1) expression in human ACL-derived cells. However, the biological function and stress-related response of CCN2/CTGF were still unclear in ACL fibroblasts. In the present study, CCN2/CTGF was observed in ACL-to-bone interface, but was not in the midsubstance region by immunohistochemical analyses. CTS treatments induced higher increase of CCN2/CTGF expression and secretion in interface cells compared with midsubstance cells. COL1A1 expression was not influenced by CCN2/CTGF treatment in interface cells despite CCN2/CTGF stimulated COL1A1 expression in midsubstance cells. However, CCN2/CTGF stimulated the proliferation of interface cells. Our results suggest that distinct biological function of stretch-induced CCN2/CTGF might regulate region-specific phenotypes of ACL-derived cells.
AB - Anterior cruciate ligament (ACL)-to-bone interface serves to minimize the stress concentrations that would arise between two different tissues. Mechanical stretch plays an important role in maintaining cell-specific features by inducing CCN family 2/connective tissue growth factor (CCN2/CTGF). We previously reported that cyclic tensile strain (CTS) stimulates α1(I) collagen (COL1A1) expression in human ACL-derived cells. However, the biological function and stress-related response of CCN2/CTGF were still unclear in ACL fibroblasts. In the present study, CCN2/CTGF was observed in ACL-to-bone interface, but was not in the midsubstance region by immunohistochemical analyses. CTS treatments induced higher increase of CCN2/CTGF expression and secretion in interface cells compared with midsubstance cells. COL1A1 expression was not influenced by CCN2/CTGF treatment in interface cells despite CCN2/CTGF stimulated COL1A1 expression in midsubstance cells. However, CCN2/CTGF stimulated the proliferation of interface cells. Our results suggest that distinct biological function of stretch-induced CCN2/CTGF might regulate region-specific phenotypes of ACL-derived cells.
KW - Anterior cruciate ligament
KW - CCN2/CTGF
KW - Collagen
KW - Cyclic tensile strain
KW - Ligament-to-bone interface
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U2 - 10.1016/j.bbrc.2011.04.138
DO - 10.1016/j.bbrc.2011.04.138
M3 - Article
C2 - 21569762
AN - SCOPUS:79957897290
SN - 0006-291X
VL - 409
SP - 247
EP - 252
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -