EFFECTS OF INTERLEUKIN-1 ON SYNTHESES OF ALKALINE-PHOSPHATASE, TYPE-X COLLAGEN, AND 1,25-DIHYDROXYVITAMIN-D(3) RECEPTOR, AND MATRIX CALCIFICATION IN RABBIT CHONDROCYTE CULTURES

被引:35
作者
KATO, Y
NAKASHIMA, K
IWAMOTO, M
MURAKAMI, H
HIRANUMA, H
KOIKE, T
SUZUKI, F
FUCHIHATA, H
IKEHARA, Y
NOSHIRO, M
JIKKO, A
机构
[1] OSAKA UNIV,FAC DENT,DEPT RADIOL,SUITA,OSAKA 565,JAPAN
[2] OSAKA UNIV,FAC DENT,DEPT BIOCHEM,SUITA,OSAKA 565,JAPAN
[3] OSAKA CITY UNIV,SCH MED,DEPT PEDIAT,OSAKA 545,JAPAN
[4] FUKUOKA UNIV,SCH MED,DEPT BIOCHEM,FUKUOKA 81401,JAPAN
关键词
MINERALIZATION; CARTILAGE; CYTOKINE; OSSIFICATION; FRACTURE;
D O I
10.1172/JCI116836
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The effect of IL-1 on expression of the mineralization-related phenotype by chondrocytes was examined. In cultures of rabbit growth plate chondrocytes, IL-1 beta at 0.1 ng / ml caused 95% decreases in alkaline phosphatase activity, alkaline phosphatase mRNA levels, the incorporation of Ca-45 into insoluble material, and the calcium content during the hypertrophic stage. These effects of IL-1 beta were dose-dependent and were observed in 24-48 h. Furthermore, IL-1 beta suppressed increase in cell size and the syntheses of 1,25-dihydroxyvitamin D3 receptor and type X collagen, other markers of hypertrophy, but had little effect on the synthesis of total protein including type II collagen. The inhibition of calcification was observed only when chondrocytes were exposed to IL-1 before the onset of calcification: IL-1 treatment from the mineralization stage had a marginal effect on Ca-45 incorporation into insoluble material. These results suggest that IL-1 inhibits chondrocyte hypertrophy and the onset of calcification in ossifying cartilage.
引用
收藏
页码:2323 / 2330
页数:8
相关论文
共 46 条
[1]   STIMULATION OF MUSCLE PROTEIN-DEGRADATION AND PROSTAGLANDIN-E2 RELEASE BY LEUKOCYTIC PYROGEN (INTERLEUKIN-1) - A MECHANISM FOR THE INCREASED DEGRADATION OF MUSCLE PROTEINS DURING FEVER [J].
BARACOS, V ;
RODEMANN, HP ;
DINARELLO, CA ;
GOLDBERG, AL .
NEW ENGLAND JOURNAL OF MEDICINE, 1983, 308 (10) :553-558
[2]  
BESSEY OA, 1946, J BIOL CHEM, V164, P321
[3]   A MODIFIED URONIC ACID CARBAZOLE REACTION [J].
BITTER, T ;
MUIR, HM .
ANALYTICAL BIOCHEMISTRY, 1962, 4 (04) :330-&
[4]   EFFECT OF A INTERLEUKIN-I LIKE FACTOR (MONONUCLEAR CELL FACTOR) ON PROTEOGLYCAN SYNTHESIS IN CULTURED HUMAN ARTICULAR CHONDROCYTES [J].
BOCQUET, J ;
DAIREAUX, M ;
LANGRIS, M ;
JOUIS, V ;
PUJOL, JP ;
BELIARD, R ;
LOYAU, G .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1986, 134 (02) :539-549
[5]   INTERLEUKIN-1 STIMULATES PROSTAGLANDIN SYNTHESIS AND CYCLIC-AMP ACCUMULATION IN SWISS 3T3 FIBROBLASTS - INTERACTIONS BETWEEN 2 2ND MESSENGER SYSTEMS [J].
BURCH, RM ;
WHITE, MF ;
CONNOR, JR .
JOURNAL OF CELLULAR PHYSIOLOGY, 1989, 139 (01) :29-33
[6]  
Cox RA., 1968, METHODS ENZYMOL, V12, P120, DOI 10.1016/0076-6879(67)12123-X
[7]   THE BIPHASIC NATURE OF RENAL CALCIFICATION [J].
DAHL, LK ;
DOLE, VP .
JOURNAL OF EXPERIMENTAL MEDICINE, 1952, 95 (04) :341-346
[8]   HUMAN RECOMBINANT INTERLEUKIN-1 STIMULATES COLLAGENASE AND PROSTAGLANDIN E-2 PRODUCTION BY HUMAN SYNOVIAL-CELLS [J].
DAYER, JM ;
DEROCHEMONTEIX, B ;
BURRUS, B ;
DEMCZUK, S ;
DINARELLO, CA .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (02) :645-648
[9]   BIOLOGY OF INTERLEUKIN-1 [J].
DINARELLO, CA .
FASEB JOURNAL, 1988, 2 (02) :108-115
[10]  
GOLDRING MB, 1987, J BIOL CHEM, V262, P16724