Matrix metalloproteinase 9 (92-kDa gelatinase/type IV collagenase) is induced in rabbit articular chondrocytes by cotreatment with interleukin 1 beta and a protein kinase C activator.
Matrix metalloproteinase 9 (92-kDa gelatinase/type IV collagenase) is induced in rabbit articular chondrocytes by cotreatment with interleukin 1 beta and a protein kinase C activator.
复制标题
通过与白细胞介素 1β 和蛋白激酶 C 激活剂共同处理，在兔关节软骨细胞中诱导基质金属蛋白酶 9（92-kDa 明胶酶/IV 型胶原酶）。
DOI：
10.1016/0014-4827(92)90271-9
复制
发表时间：
1992
影响因子：
3.7
通讯作者：
Arner,EC
中科院分区：
文献类型：
--
作者：
Ogata,Y;Pratta,MA;Nagase,H;Arner,EC
通过与重组白细胞介素 1β (rIL-1β) 和蛋白激酶 C (PKC) 激动剂佛波醇 12,13-二丁酸酯 (PDBu) 或 mezerein 共处理，在兔关节软骨细胞的原代培养物中诱导合成 88 kDa 明胶分解酶，该酶被鉴定为基质金属蛋白酶 (proMMP)-9 的酶原。未刺激的细胞或单独用浓度高达 100 ng/ml 的 PKC 激活剂处理的细胞产生的 88-kDa 明胶分解活性可忽略不计，单独使用 rIL-1β 在浓度 1-100 ng/ml 时仅产生适度的诱导作用。然而，当这些细胞在 IL-1β (1 ng/ml) 存在的情况下用 PKC 激活剂处理时，诱导作用是惊人的，在浓度低至 1 ng/ml 的 mezerein 或 10 ng/ml 的 PDBu 时即可检测到酶活性。培养的兔软骨细胞组成型产生 MMP-2 (proMMP-2) 酶原，并且单独或联合使用 IL-1β 或 PKC 激动剂处理不会改变其产量。在 PKC 激活剂存在的情况下，重组肿瘤坏死因子 α (rTNFα) 不能替代 IL-1β 诱导 proMMP-9，单独使用 IL-1β 或 TNFα 也无效。这些数据表明，兔关节软骨细胞在某些生物学和病理条件下具有合成和分泌proMMP-9的潜力，但proMMP-9的表达与其他MMP的表达调控不同。
The synthesis of an 88-kDa gelatinolytic enzyme, identified as a zymogen of matrix metalloproteinase (proMMP)-9, was induced in the primary culture of rabbit articular chondrocytes by cotreatment with recombinant interleukin 1β (rIL-1β) and the protein kinase C (PKC) agonists, phorbol 12,13-dibutyrate (PDBu) or mezerein. Negligible 88-kDa gelatinolytic activity was produced by unstimulated cells or cells treated with a PKC activator alone at concentrations up to 100 ng/ml, and only a modest induction occurred with rIL-1β alone at concentrations of 1–100 ng/ml. However, when these cells were treated with a PKC activator in the presence of IL-1β (1 ng/ml), induction was striking, with enzymic activity detectable at a concentration as low as 1 ng/ml of mezerein or 10 ng/ml of PDBu. Rabbit chondrocytes in culture constitutively produced the zymogen of MMP-2 (proMMP-2) and its production was not altered by treatment with IL-1β or PKC agonists alone or in combination. Recombinant tumor necrosis factor α (rTNFα) did not substitute for IL-1β in inducing proMMP-9 in the presence of PKC activators, nor was the combination of IL-1β or TNFα alone effective. These data indicate that rabbit articular chondrocytes have a potential to synthesize and secrete proMMP-9 under certain biological and pathological conditions but that the expression of proMMP-9 is differently regulated from that of other MMPs.