白细胞介素-1与纤维蛋白溶解系统在关节软骨细胞降解胶原蛋白过程中的协同作用。

Co-operation between interleukin-1 and the fibrinolytic system in the degradation of collagen by articular chondrocytes.

作者信息

Cruwys S C, Davies D E, Pettipher E R

机构信息

Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent.

出版信息

Br J Pharmacol. 1990 Jul;100(3):631-5. doi: 10.1111/j.1476-5381.1990.tb15858.x.

DOI:10.1111/j.1476-5381.1990.tb15858.x

PMID:2167739

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1917795/

Abstract

The interaction between interleukin 1 (IL-1) and the fibrinolytic system in the control of collagen degradation by rabbit chondrocytes has been investigated in a tissue-culture system where cells are grown on a 14C-labelled collagen matrix. 2. Culture of rabbit chondrocytes in the presence of human recombinant IL-1 beta at a concentration of 57pM for 48 h led to the presence of procollagenase but not active collagenase in the medium. The latent collagenase could be activated by incubation with an organomercurial, aminophenylmercuric acetate (APMA). 3. Addition of IL-1 beta to chondrocytes grown on a 14C-labelled collagen matrix did not increase the degradation of the matrix compared to control over a 48 h period. However, in the presence of plasmin (200 micrograms ml-1) or plasminogen (100 micrograms ml-1), IL-1 beta (57 pM) caused almost complete degradation of the collagen matrix. Plasmin or plasminogen alone caused only slight degradation of the collagen matrix. 4. Tissue inhibitor of metalloproteinases (TIMP) or the selective metalloproteinase inhibitor, SC44463, inhibited the degradation induced by IL-1 beta and plasminogen in a concentration-related manner and at concentrations that were correlated with inhibition of collagenase. 5. When concentrations of IL-1 beta which caused only minimal degradation of the matrix in the presence of plasminogen were combined with fibrin (1 microgram ml-1), there was almost total degradation of the matrix by 48 h. 6. These results indicate there is a synergistic interaction between IL-1 and the fibrinolytic system in the degradation of collagen by rabbit chondrocytes in culture.

摘要

在一个细胞生长于14C标记的胶原基质上的组织培养系统中，研究了白细胞介素1（IL-1）与纤维蛋白溶解系统在兔软骨细胞控制胶原降解过程中的相互作用。2. 在含有浓度为57pM的人重组IL-1β的条件下培养兔软骨细胞48小时，导致培养基中存在前胶原酶但不存在活性胶原酶。潜伏的胶原酶可通过与有机汞化合物醋酸氨基苯基汞（APMA）孵育而被激活。3. 与对照组相比，在48小时内，向生长于14C标记胶原基质上的软骨细胞添加IL-1β并没有增加基质的降解。然而，在纤溶酶（200微克/毫升）或纤溶酶原（100微克/毫升）存在的情况下，IL-1β（57pM）导致胶原基质几乎完全降解。单独的纤溶酶或纤溶酶原仅引起胶原基质轻微降解。4. 金属蛋白酶组织抑制剂（TIMP）或选择性金属蛋白酶抑制剂SC44463以浓度相关的方式抑制IL-1β和纤溶酶原诱导的降解，且其浓度与胶原酶抑制相关。5. 当在纤溶酶原存在下仅引起基质最小降解的IL-1β浓度与纤维蛋白（1微克/毫升）联合使用时，到48小时时基质几乎完全降解。6. 这些结果表明，在培养的兔软骨细胞胶原降解过程中，IL-1与纤维蛋白溶解系统之间存在协同相互作用。