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软骨细胞中的自发振荡和机械诱导钙波

Spontaneous oscillation and mechanically induced calcium waves in chondrocytes.

作者信息

Kono Taisuke, Nishikori Tetsuya, Kataoka Hiroko, Uchio Yuji, Ochi Mitsuo, Enomoto Koh-ichi

机构信息

Department of Orthopaedics, Faculty of Medicine, Shimane University, Izumo-shi, Shimane, Japan.

出版信息

Cell Biochem Funct. 2006 Mar-Apr;24(2):103-11. doi: 10.1002/cbf.1304.

Abstract

The characteristics of spontaneous calcium (Ca(2+)) oscillation and mechanically induced Ca(2+) waves in articular chondrocytes were studied. In some, but not all, chondrocytes in sliced cartilage and primary cultures, we observed spontaneous oscillation of intracellular Ca(2+) that never spread to adjacent cells. In contrast, a mechanical stimulus to a single cell by touching with a glass rod induced an increase of intracellular Ca(2+) that spread to neighboring cells in a wave-like manner, even though there was no physical contact between the cells. This indicated the release of some paracrine factor from the mechanically stimulated cells. Application of ultrasonic vibration also induced an oscillation of intracellular Ca(2+). The application of a uridine 5'-triphosphate (UTP), UTP, induced a transient increase in intracellular Ca(2+) and the release of adenosine 5'-triphosphate (ATP) in cultured chondrocytes. A P2 receptor antagonist (suramin) and blockers of Cl(-) channels, niflumic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), reduced the UTP-induced ATP release. The results indicated that Cl(-) channels were involved in the extracellular release of ATP following mechanical or P2Y receptor stimulation. Thus, ATP stimulation of P2Y receptors elicits an increase in intracellular Ca(2+), triggering further release of ATP from adjacent cells, thereby expanding the Ca(2+) wave in chondrocytes.

摘要

研究了关节软骨细胞中自发钙(Ca(2+))振荡和机械诱导的Ca(2+)波的特征。在切片软骨和原代培养物中的部分(而非全部)软骨细胞中,我们观察到细胞内Ca(2+)的自发振荡,且这种振荡从未扩散到相邻细胞。相反,用玻璃棒触碰对单个细胞施加机械刺激会诱导细胞内Ca(2+)增加,并以波状方式扩散到邻近细胞,即便细胞之间没有物理接触。这表明机械刺激的细胞释放了某种旁分泌因子。施加超声振动也会诱导细胞内Ca(2+)振荡。在培养的软骨细胞中,施加尿苷5'-三磷酸(UTP)会诱导细胞内Ca(2+)短暂增加以及腺苷5'-三磷酸(ATP)释放。P2受体拮抗剂(苏拉明)以及Cl(-)通道阻滞剂尼氟酸和4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)可减少UTP诱导的ATP释放。结果表明,Cl(-)通道参与了机械刺激或P2Y受体刺激后ATP的细胞外释放。因此,P2Y受体的ATP刺激会引发细胞内Ca(2+)增加,触发相邻细胞进一步释放ATP,从而在软骨细胞中扩大Ca(2+)波。

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