Relaxin modulates the expression of MMPs and TIMPs in fibroblasts of patients with carpal tunnel syndrome

Young Mi Kang; Hwan Mo Lee; Seong Hwan Moon; Ho Kang; Yun Rak Choi

doi:10.3349/ymj.2017.58.2.415

Relaxin modulates the expression of MMPs and TIMPs in fibroblasts of patients with carpal tunnel syndrome

Young Mi Kang, Hwan Mo Lee, Seong Hwan Moon, Ho Kang, Yun Rak Choi

Department of Orthopaedic Surgery

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

Abstract

Purpose: The aim of this study was to investigate the anti-fibrotic effect of relaxin in subsynovial fibroblasts activated by transforming growth factor beta (TGF-β). Materials and Methods: To test the anti-fibrotic effect of an adenovirus-relaxin construct (Ad-RLN) on subsynovial fibroblasts in vitro, cells from subsynovial connective tissue of patients with carpal tunnel syndrome were activated with TGF-β1 and exposed to Ad-RLN (as a therapeutic gene) or adenovirus-lacZ construct (as a marker gene) for four hours. Subsynovial fibroblast cultures without adenoviral exposure served as controls. Results: We observed induction of gene expressions of collagen I, III and IV, as well as the abatement of alpha-smooth muscle actin (a-SMA) synthesis, Smad2 phosphorylation, and fibronectin at the protein level, in comparison to controls. In addition, protein expressions of matrix metalloproteinase (MMP) I was significantly induced, whereas the protein expressions of tissue inhibitor of metalloproteinases (TIMP) I and IV were reduced due to relaxin expression. Conclusion: RLN prevents excessive synthesis of extracellular matrix by reducing the expressions of its components, such as fibronectin, a-SMA, and phosphorylated Smad2, by increasing the expression of MMPs; and by decreasing the expression of TIMPs.

Original language	English
Pages (from-to)	415-422
Number of pages	8
Journal	Yonsei medical journal
Volume	58
Issue number	2
DOIs	https://doi.org/10.3349/ymj.2017.58.2.415
Publication status	Published - 2017 Mar

Bibliographical note

Funding Information:
We would like to thank Chae-Ok Yun, Ph.D. (Department of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea) for providing the adenovirus-relaxin construct. This work was supported, in part, by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. This study was supported by a faculty research program from Yonsei University College of Medicine (6-2014-0098), as well as the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (grant number: 2011-0014399).

All Science Journal Classification (ASJC) codes

Medicine(all)

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@article{fbf2663115754d40b765ff77a4e98f2b,

title = "Relaxin modulates the expression of MMPs and TIMPs in fibroblasts of patients with carpal tunnel syndrome",

abstract = "Purpose: The aim of this study was to investigate the anti-fibrotic effect of relaxin in subsynovial fibroblasts activated by transforming growth factor beta (TGF-β). Materials and Methods: To test the anti-fibrotic effect of an adenovirus-relaxin construct (Ad-RLN) on subsynovial fibroblasts in vitro, cells from subsynovial connective tissue of patients with carpal tunnel syndrome were activated with TGF-β1 and exposed to Ad-RLN (as a therapeutic gene) or adenovirus-lacZ construct (as a marker gene) for four hours. Subsynovial fibroblast cultures without adenoviral exposure served as controls. Results: We observed induction of gene expressions of collagen I, III and IV, as well as the abatement of alpha-smooth muscle actin (a-SMA) synthesis, Smad2 phosphorylation, and fibronectin at the protein level, in comparison to controls. In addition, protein expressions of matrix metalloproteinase (MMP) I was significantly induced, whereas the protein expressions of tissue inhibitor of metalloproteinases (TIMP) I and IV were reduced due to relaxin expression. Conclusion: RLN prevents excessive synthesis of extracellular matrix by reducing the expressions of its components, such as fibronectin, a-SMA, and phosphorylated Smad2, by increasing the expression of MMPs; and by decreasing the expression of TIMPs.",

author = "Kang, {Young Mi} and Lee, {Hwan Mo} and Moon, {Seong Hwan} and Ho Kang and Choi, {Yun Rak}",

note = "Funding Information: We would like to thank Chae-Ok Yun, Ph.D. (Department of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea) for providing the adenovirus-relaxin construct. This work was supported, in part, by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. This study was supported by a faculty research program from Yonsei University College of Medicine (6-2014-0098), as well as the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (grant number: 2011-0014399).",

year = "2017",

month = mar,

doi = "10.3349/ymj.2017.58.2.415",

language = "English",

volume = "58",

pages = "415--422",

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AU - Kang, Young Mi

AU - Lee, Hwan Mo

AU - Moon, Seong Hwan

AU - Kang, Ho

AU - Choi, Yun Rak

N1 - Funding Information: We would like to thank Chae-Ok Yun, Ph.D. (Department of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea) for providing the adenovirus-relaxin construct. This work was supported, in part, by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. This study was supported by a faculty research program from Yonsei University College of Medicine (6-2014-0098), as well as the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (grant number: 2011-0014399).

PY - 2017/3

Y1 - 2017/3

N2 - Purpose: The aim of this study was to investigate the anti-fibrotic effect of relaxin in subsynovial fibroblasts activated by transforming growth factor beta (TGF-β). Materials and Methods: To test the anti-fibrotic effect of an adenovirus-relaxin construct (Ad-RLN) on subsynovial fibroblasts in vitro, cells from subsynovial connective tissue of patients with carpal tunnel syndrome were activated with TGF-β1 and exposed to Ad-RLN (as a therapeutic gene) or adenovirus-lacZ construct (as a marker gene) for four hours. Subsynovial fibroblast cultures without adenoviral exposure served as controls. Results: We observed induction of gene expressions of collagen I, III and IV, as well as the abatement of alpha-smooth muscle actin (a-SMA) synthesis, Smad2 phosphorylation, and fibronectin at the protein level, in comparison to controls. In addition, protein expressions of matrix metalloproteinase (MMP) I was significantly induced, whereas the protein expressions of tissue inhibitor of metalloproteinases (TIMP) I and IV were reduced due to relaxin expression. Conclusion: RLN prevents excessive synthesis of extracellular matrix by reducing the expressions of its components, such as fibronectin, a-SMA, and phosphorylated Smad2, by increasing the expression of MMPs; and by decreasing the expression of TIMPs.

AB - Purpose: The aim of this study was to investigate the anti-fibrotic effect of relaxin in subsynovial fibroblasts activated by transforming growth factor beta (TGF-β). Materials and Methods: To test the anti-fibrotic effect of an adenovirus-relaxin construct (Ad-RLN) on subsynovial fibroblasts in vitro, cells from subsynovial connective tissue of patients with carpal tunnel syndrome were activated with TGF-β1 and exposed to Ad-RLN (as a therapeutic gene) or adenovirus-lacZ construct (as a marker gene) for four hours. Subsynovial fibroblast cultures without adenoviral exposure served as controls. Results: We observed induction of gene expressions of collagen I, III and IV, as well as the abatement of alpha-smooth muscle actin (a-SMA) synthesis, Smad2 phosphorylation, and fibronectin at the protein level, in comparison to controls. In addition, protein expressions of matrix metalloproteinase (MMP) I was significantly induced, whereas the protein expressions of tissue inhibitor of metalloproteinases (TIMP) I and IV were reduced due to relaxin expression. Conclusion: RLN prevents excessive synthesis of extracellular matrix by reducing the expressions of its components, such as fibronectin, a-SMA, and phosphorylated Smad2, by increasing the expression of MMPs; and by decreasing the expression of TIMPs.

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