RETRACTED: The influence of connective tissue growth factor on rabbit ligament injury repair (Retracted article. See vol. 28, pg. 637, 2020)

被引：5
|
作者：
Zhang, Wei [1 ]
Zheng, Junju [1 ]
Chen, Jiayu [2 ]
Huang, Lipeng [1 ]
机构：
[1] WenZhou Cent Hosp, Dept Orthoped, Wenzhou 325000, Zhejiang, Peoples R China
[2] Shaoxing Univ, Sch Med, Shaoxing 312000, Zhejiang, Peoples R China
来源：
SAUDI PHARMACEUTICAL JOURNAL | 2017年 / 25卷 / 04期
关键词：
Anterior cruciate ligament; Connective tissue growth factor; TGF-beta; 1; mRNA; Rabbit; ANTERIOR CRUCIATE LIGAMENT; CCN FAMILY; EXPRESSION; PROLIFERATION; PROTEINS; FIBROSIS; CELLS; CTGF;
D O I：
10.1016/j.jsps.2017.04.013
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Objectives: The injured anterior cruciate ligament (ACL) is deemed to exhibit an impaired healing response and attempts at surgical repair have not been successful. Connective tissue growth factor (CTGF) is reported to be associated with wound healing, probably through transforming growth factor beta1 (TGF-beta 1). Methods: A rabbit ACL injury model was used to study the effect of CTGF on ligament recovery. Quantitative real-time PCR was performed for detection of changes in RNA levels of TGF-beta 1, type 1 collagen (COL-I), type 2 collagen (COL-II), SRY-related high mobility group-box gene9 (Sox9), metalloproteinase-1 (TIMP-1) as well as matrix metallopeptidase 13 (MMP-13). And expression of related proteins was detected by western blotting. Results: The current study showed that CTGF could promote the recovery of inured anterior cruciate ligament. It can up-regulate the mRNA and expression of TGF-beta 1, COL-I, COL-II, Sox9, as well as the tissue inhibitor of TIMP-1, and down-regulated the mRNA and expression of MMP-13, suggesting the curative effect of CTGF on injured rabbit ligament is through regulating these cellular factors. Conclusion: This finding revealed the mechanism of CTFG's healing role in injured tissues and provided new possibilities of treating injured tissues and wound healing by using CTFG. (C) 2017 Production and hosting by Elsevier B.V. on behalf of King Saud University.
引用
收藏
页码：498 / 503
页数：6
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