Luo L, Cruz T, McCulloch C
MRC Group in Periodontal Physiology, Medical Sciences Building, 8 Taddle Creek Road, Toronto, Ontario, Canada M5G 1G6.
Biochem J. 1997 Jun 1;324 ( Pt 2)(Pt 2):653-8. doi: 10.1042/bj3240653.
The cytokine interleukin 1 (IL-1) is an important mediator of connective-tissue destruction in arthritic joints but the mechanisms by which IL-1 mediates signal transduction in chondrocytes is poorly understood. Previous results have indicated that IL-1 receptors co-localize with focal adhesions [Qwarnstrom, Page, Gillis and Dower (1988) J. Biol. Chem. 263, 8261-8269], discrete adhesive domains of cells that function in cell attachment and possibly in signal transduction. We have determined whether focal adhesions restrict IL-1-induced Ca2+ signalling in primary cultures of bovine chondrocytes. In cells grown for 24 h on fibronectin, the basal intracellular Ca2+ ion concentration ([Ca2+]i) was 100+/-3 nM. Optimal increases of [Ca2+]i above baseline were induced by 10 nM IL-1 (183+/-30 nM above baseline). There was no significant difference between cells plated on fibronectin or type II collagen (P>0.2; 233+/-90 nM above baseline). Ca2+ transients were significantly decreased by the inclusion of 0.5 mM EGTA in the bathing buffer (74+/-11 nM above baseline), and 1 microM thapsigargin completely blocked Ca2+ transients. Cells plated on poly-(l-lysine) or suspended cells showed no Ca2+ increases, whereas cells grown on fibronectin exhibited IL-1-induced Ca2+ responses that corresponded temporally to the time-dependent cell spreading after plating on fibronectin. Cells plated on poly-(l-lysine) and incubated with fibronectin-coated beads exhibited vinculin staining in association with the beads. In identical cell preparations, IL-1 induced a 136+/-39 nM increase of [Ca2+]i above baseline in response to 10 nM IL-1beta. There were no IL-1-induced Ca2+ increases when cells on poly-(l-lysine) were incubated with fibronectin-coated beads for only 15 min at 37 degrees C, in cells maintained for 3 h at 4 degrees C, in cells incubated with BSA beads for 3 h at 37 degrees C, or in cells pretreated with cytochalasin D. Labelling of IL-1 receptors with 125I-IL-1beta showed 3-fold more specific labelling of focal adhesion complexes in cells incubated with fibronectin-coated beads compared with cells incubated with BSA-coated beads, indicating that IL-1 receptor binding or the number of IL-1 receptors was increased in focal adhesions. These results indicate that, in chondrocytes, IL-1-induced Ca2+ signalling is dependent on focal adhesion formation and that focal adhesions recruit IL-1 receptors by redistribution in the cell membrane.
细胞因子白细胞介素1(IL-1)是关节炎关节中结缔组织破坏的重要介质,但IL-1在软骨细胞中介导信号转导的机制尚不清楚。先前的结果表明,IL-1受体与粘着斑共定位[Qwarnstrom、Page、Gillis和Dower(1988年)《生物化学杂志》263,8261 - 8269],粘着斑是细胞中离散的粘附结构域,在细胞附着以及可能的信号转导中发挥作用。我们已经确定粘着斑是否会限制牛软骨细胞原代培养物中IL-1诱导的Ca2+信号传导。在纤连蛋白上生长24小时的细胞中,基础细胞内Ca2+离子浓度([Ca2+]i)为100±3 nM。10 nM IL-1诱导[Ca2+]i比基线水平最佳增加(比基线高183±30 nM)。接种在纤连蛋白或II型胶原上的细胞之间没有显著差异(P>0.2;比基线高233±90 nM)。在浴液缓冲液中加入0.5 mM EGTA可使Ca2+瞬变显著降低(比基线高74±11 nM),1 μM毒胡萝卜素完全阻断Ca2+瞬变。接种在聚-L-赖氨酸上的细胞或悬浮细胞未显示Ca2+增加,而在纤连蛋白上生长的细胞表现出IL-1诱导的Ca2+反应,其在时间上与接种在纤连蛋白上后细胞的时间依赖性铺展相对应。接种在聚-L-赖氨酸上并与纤连蛋白包被的珠子一起孵育的细胞显示与珠子相关的纽蛋白染色。在相同的细胞制剂中,10 nM IL-1β可诱导[Ca2+]i比基线水平增加136±39 nM。当接种在聚-L-赖氨酸上的细胞与纤连蛋白包被的珠子在37℃仅孵育15分钟、在4℃维持3小时、与牛血清白蛋白(BSA)珠子在37℃孵育3小时或用细胞松弛素D预处理的细胞中,没有IL-1诱导的Ca2+增加。用125I-IL-1β标记IL-1受体显示,与用BSA包被的珠子孵育的细胞相比,用纤连蛋白包被的珠子孵育的细胞中粘着斑复合物的特异性标记多3倍,表明粘着斑中IL-1受体结合或IL-1受体数量增加。这些结果表明,在软骨细胞中,IL-1诱导的Ca2+信号传导依赖于粘着斑的形成,并且粘着斑通过在细胞膜中的重新分布募集IL-1受体。