Relationship between synovial fluid ARGS-aggrecan fragments, cytokines, MMPs, and TIMPs following acute ACL injury: A cross-sectional study.
Relationship between synovial fluid ARGS-aggrecan fragments, cytokines, MMPs, and TIMPs following acute ACL injury: A cross-sectional study.
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急性 ACL 损伤后滑液 ARGS-聚集蛋白聚糖片段、细胞因子、MMP 和 TIMP 之间的关系：一项横断面研究。
DOI：
10.1002/jor.22961
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Beynnon,BruceD
中科院分区：
文献类型：
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作者：
Tourville,TimothyW;Poynter,MatthewE;DeSarno,MichaelJ;Struglics,André;Beynnon,BruceD
严重的膝关节创伤（如ACL破坏）会导致聚集蛋白聚糖降解，表现为滑液（SF）N-末端（393）丙氨酸-精氨酸-甘氨酸-丝氨酸（ARGS）新表位（或ARGS-聚集蛋白聚糖）升高，并与损伤后不久的炎症活动相关。然而，不知道这个过程是否在最初的创伤后持续了相当长的时间间隔。本研究的目的是评价前交叉韧带断裂后最初6个月内SF ARGS浓度与一系列细胞因子、基质金属蛋白酶（MMP）和金属蛋白酶组织抑制剂（TIMP）之间的关系。在手术ACL重建前6个月（18-155天）内分析了67例ACL损伤受试者（29名女性）的SF样本。评价了ARGS与单个分析物浓度以及MMP/TIMP比值之间的关系。发现ARGS与碱性成纤维细胞生长因子（FGF 2）（p= 0.03）和TIMP-3（p= 0.01）之间存在统计学显著相关性。我们的研究结果表明，FGF 2，被认为是主要在关节软骨中分解代谢，并没有下调ARGS浓度随着时间的推移，因为受伤。此外，这些结果支持了以下假设，即主要聚集蛋白聚糖酶抑制剂TIMP-3的上调是响应于聚集蛋白聚糖降解增加而引起的，这可能抑制进一步的切割。© 2015骨科研究学会。由威利期刊公司出版J Orthop Res 33：1796-1803，2015.
Severe knee trauma, such as an ACL disruption, produces aggrecan degradation as evidenced by elevated synovial fluid (SF) N‐terminal (393) Alanine–Arginine–Glycine–Serine (ARGS) neoepitope (or ARGS‐aggrecan) and is associated with inflammatory activity soon after injury. However, it is not known if this process persists for a substantial time interval following the initial trauma. The purpose of this study was to evaluate relationships between SF ARGS concentrations and an array of cytokines, matrix metalloproteases (MMPs), and tissue inhibitor of metalloproteases (TIMPs) during the initial 6 months following ACL rupture. SF samples from 67 ACL‐injured subjects (29 women) were analyzed within 6 months of injury (18–155 days), immediately prior to surgical ACL reconstruction. Relationships between ARGS and individual analyte concentrations, as well as MMP/TIMP ratios were evaluated. Statistically significant relationships were found between ARGS and basic fibroblast growth factor (FGF2) (p= 0.03) and TIMP‐3 (p= 0.01). Our findings suggest that FGF2, considered to be primarily catabolic in articular cartilage, is not downregulated as ARGS concentration declines over time since injury. In addition, these results support the hypothesis that an upregulation of TIMP‐3, the primary aggrecanase inhibitor, is elicited in response to increased aggrecan degradation, which may inhibit further cleavage. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1796–1803, 2015.