INTERLEUKIN-1 INCREASES THE PRODUCTION OF COLLAGENASE BUT DOES NOT INFLUENCE THE PHAGOCYTOSIS OF COLLAGEN FIBRILS

被引:27
作者
EVERTS, V
WOLVIUS, E
SAKLATVALA, J
BEERTSEN, W
机构
[1] STRANGEWAYS RES LAB,CAMBRIDGE CB1 4RN,ENGLAND
[2] UNIV AMSTERDAM,ACAD CTR DENT AMSTERDAM,DEPT PERIODONTOL,AMSTERDAM,NETHERLANDS
来源
MATRIX | 1990年 / 10卷 / 06期
关键词
COLLAGEN; COLLAGEN PHAGOCYTOSIS; COLLAGENASE; FIBROBLASTS; INTERLEUKIN-1;
D O I
10.1016/S0934-8832(11)80146-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of the present study was to determine whether interleukin 1-alpha-(Il-1), a cytokine known to have a stimulatory effect on collagenase production, also influences the phagocytosis and intracellular digestion of collagen fibrils by fibroblasts. Mouse long bones and calvariae both with surrounding periosteum were cultured for 24 or 48 hours in media containing varying concentrations of the cytokine. The periostea were subjected to morphometric analysis in order to assess the volume density of phagocytosed collagen fibrils in fibroblasts. The results indicated that neither in calvarial nor in long bone periosteum the uptake and intracellular degradation of collagen by fibroblasts was influenced by Il-1. However, between both tissues the amount of collagen phagocytosed differed considerably. It appeared that within 48 hours periosteal fibroblasts of calvariae ingested at least three times more fibrillar collagen than those of long bone periosteum. This finding suggests intrinsic differences between these connective tissues as to the phagocytic behaviour of the fibroblasts. Analysis of collagenase activity in the media demonstrated that under the influence of Il-1 collagenase release increased about 1.5- to 2-fold, most of the enzyme being in a latent form. The media is also proved to contain an inhibitor of collagenase, its production not being affected by Il-1. It is concluded that under the conditions tested Il-1 does not seem to play a role in the regulation of the intracellular pathway of collagen digestion.
引用
收藏
页码:388 / 393
页数:6
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