Connective tissue growth factor is expressed by a subset of reactive astrocytes in human cerebral infarction
Connective tissue growth factor is expressed by a subset of reactive astrocytes in human cerebral infarction
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DOI：
10.1046/j.1365-2990.2000.00271.x
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发表时间：
2000-10-01
影响因子：
5
通讯作者：
Schluesener, HJ
中科院分区：
文献类型：
--
作者：
Schwab, JM;Postler, E;Schluesener, HJ
结缔组织生长因子（CTGF）是一种转化生长因子（TGF）-β（1）下游介质，是一种分泌的细胞基质诱导肽，其参与组织再生机制（如伤口修复）以及细胞外基质的异常沉积。本研究报告CTGF表达的细胞与基质沉积和胶质瘢痕形成在人类脑梗死。CTGF定位于17例局灶性脑梗死患者的大脑和三个神经病理正常对照组的大脑。CTGF表达选择性定位于星形反应性星形胶质细胞的细胞质。与周围区域和无神经病理学发现的脑对照相比，CTGF（+）星形胶质细胞的总数在邻近核心的边缘区（对应于半暗带）显著更高（P < 0.0001）。这些数字在第1天和第3天显著增加，并持续升高至梗死后几个月（P < 0.0001）。CTGF（+）反应性星形胶质细胞的有限表达和积累为CTGF参与胶质瘢痕形成中的胶质星形胶质细胞CNS损伤反应提供了令人信服的证据。CTGF可以被认为是早期人类星形胶质细胞活化的敏感标志物，并且是异常基质沉积的药物干预的可能靶点。
Connective tissue growth factor (CTGF), a transforming growth factor (TGF)-beta(1) downstream mediator, is a secreted cell matrix-inducing peptide involved in both tissue regeneration mechanisms, such as wound repair, and also in aberrant deposition of extracellular matrix. The present study reports CTGF expression by cells associated with matrix deposition and glial scar formation in human cerebral infarction. CTGF was localized by immunohistochemistry in 17 brains of patients after focal infarction and in three neuropathologically normal control brains. CTGF expression was selectively localized to the cytoplasm of stellate reactive astrocytes. Compared to peripheral areas and brain controls without neuropathological findings, the total number CTGF(+) astrocytes was significantly higher (P < 0.0001) in border zones adjacent to the core, corresponding to the penumbra. These numbers were significantly increased at day 1 and day 3 and remained persistently elevated up to several months post-infarction (P < 0.0001). The restricted expression and accumulation of CTGF(+) reactive astrocytes adds convincing evidence for CTGF participation in the gliotic astrocyte CNS injury response involved in glial scar formation. CTGF can be considered a sensitive marker of early human astrocyte activation and a possible target for pharmacological intervention of aberrant matrix deposition.