Dynamics of MMP‑9, MMP‑2 and TIMP‑1 in a rat model of brain injury combined with traumatic heterotopic ossification

脑损伤合并创伤性异位骨化大鼠模型中 MMP-9、MMP-2 和 TIMP-1 的动态变化

阅读:7
作者:Wei-Zhe Shi, Jin-Yong Ju, Hai-Jun Xiao, Feng Xue, Jiang Wu, Ming-Mang Pan, Wei-Feng Ni

Abstract

The present study aimed to detect early changes in the concentration of matrix metalloproteinase-9 (MMP-9), matrix metalloproteinase‑2 (MMP‑2) and tissue inhibitor of metalloproteinase‑1 (TIMP‑1) in a rat model of brain injury combined with traumatic heterotopic ossification (HO). A total of 132 male Sprague‑Dawley rats were used to establish the experimental and control groups. Anatomy and sample collection were conducted on postoperative days 1, 2, 3, 4, 5, 6 and 7. Hematoxylin and eosin and immunohistochemical staining were performed for local tissues. MMP‑9, MMP‑2 and TIMP‑1 levels and gene expression level were measured by ELISA and reverse transcription‑quantitative polymerase chain reaction. Radiological investigation of the rat lower limbs was conducted at weeks 5 and 10 following modeling to observe the occurrence of HO. The incidence of HO for rats in the experimental group was higher compared with the control group. The serum MMP‑9 levels of the experimental group were notably higher on postoperative days 5‑7 compared with the control group. The MMP‑9 gene expression of the experimental group was higher on postoperative days 3‑7 compared with the control group. The TIMP‑1 gene expression levels were markedly higher compared with the control group at each time point. Thus, an increase in inflammatory response is closely associated with brain injury, in addition to an increase in the number of inflammatory cells with the incidence of HO. The pathological elevation of MMP‑9 and the altered dynamic equilibrium between MMP‑9 and TIMP‑1 contributed to the degradation, remodeling and calcification of the extracellular matrix, resulting in the induction of osteoblast precursor cells in HO. MMP‑9 is a predictive marker of HO.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。