钙在大鼠少突胶质细胞损伤与修复中的作用。

The role of calcium in rat oligodendrocyte injury and repair.

作者信息

Scolding N J, Morgan B P, Campbell A K, Compston D A

机构信息

University of Cambridge Neurology Unit, Addenbrooke's Hospital, U.K.

出版信息

Neurosci Lett. 1992 Jan 20;135(1):95-8. doi: 10.1016/0304-3940(92)90144-v.

DOI:10.1016/0304-3940(92)90144-v

PMID:1542444

Abstract

The role of intracellular calcium in oligodendrocyte injury is investigated using cultured rat oligodendrocytes. Calcium ionophores A23187 and ionomycin mimic both complement and perforin attack, causing oligodendrocyte lysis at concentrations which do not lyse other glia. Membrane vesiculation, the mechanism by which oligodendrocytes resist and recover from complement and perforin attack, is also induced by A23187. Oligodendrocytes are more susceptible to complement attack in the presence of a calmodulin inhibitor (W7), which also inhibits vesiculation. These results imply that calmodulin is involved in membrane repair from complement attack, and indicate that changes in intracellular calcium play an important yet paradoxical role in the oligodendrocyte response to injury, dictating both susceptibility and cellular recovery.

摘要

利用培养的大鼠少突胶质细胞研究细胞内钙在少突胶质细胞损伤中的作用。钙离子载体A23187和离子霉素模拟补体和穿孔素攻击，在不裂解其他神经胶质细胞的浓度下导致少突胶质细胞裂解。膜泡形成是少突胶质细胞抵抗补体和穿孔素攻击并从中恢复的机制，A23187也可诱导膜泡形成。在存在钙调蛋白抑制剂（W7）的情况下，少突胶质细胞对补体攻击更敏感，W7也抑制膜泡形成。这些结果表明钙调蛋白参与补体攻击后的膜修复，并表明细胞内钙的变化在少突胶质细胞对损伤的反应中起重要但矛盾的作用，决定了易感性和细胞恢复能力。