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细胞因子诱导培养的人星形胶质细胞产生巨噬细胞炎性蛋白-1α(MIP-1α)

Cytokine-induced production of macrophage inflammatory protein-1alpha (MIP-1alpha) in cultured human astrocytes.

作者信息

Miyamoto Y, Kim S U

机构信息

Department of Medicine, University of British Columbia, Vancouver, Canada.

出版信息

J Neurosci Res. 1999 Jan 15;55(2):245-51. doi: 10.1002/(SICI)1097-4547(19990115)55:2<245::AID-JNR12>3.0.CO;2-Q.

DOI:10.1002/(SICI)1097-4547(19990115)55:2<245::AID-JNR12>3.0.CO;2-Q
PMID:9972827
Abstract

Macrophage inflammatory protein-1alpha (MIP-1alpha) is a member of a superfamily of inflammatory cytokines termed chemokines, and it has been implicated in the pathogenesis of several human diseases with inflammatory components. It has been known that MIP-1alpha plays a role in recruiting and activating mononuclear phagocytes in the central nervous system (CNS), and that astrocytes and microglia are sources of this chemokine. However, details of the regulation of MIP-1alpha production by these glial cells are not known. In the present study, expression of MIP-1alpha was determined in purified cultures of human astrocyte. MIP-1alpha mRNA levels in human astrocyte cell preparations were determined by reverse transcription polymerase chain reaction (RT-PCR) and amount of MIP-1alpha protein secreted into culture supernatants by human astrocytes was assayed by enzyme-linked immunosorbent assay (ELISA). Under the unstimulated conditions, human astrocytes did not express MIP-1alpha message or protein, indicating that human astrocytes do not constitutively carry MIP-1alpha message. Following treatment with interleukin-1beta (IL-1beta), human astrocytes demonstrated increased message and protein expression for MIP-1alpha, while other immune modulators such as interferon-gamma (IFN)-gamma, tumor necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), lipopolysaccharide, or phorbol ester (a protein kinase C activator) did not induce MIP-1alpha expression in human astrocytes.

摘要

巨噬细胞炎性蛋白-1α(MIP-1α)是被称为趋化因子的炎性细胞因子超家族的一员,它与几种具有炎症成分的人类疾病的发病机制有关。已知MIP-1α在中枢神经系统(CNS)中募集和激活单核吞噬细胞方面发挥作用,并且星形胶质细胞和小胶质细胞是这种趋化因子的来源。然而,这些神经胶质细胞对MIP-1α产生的调节细节尚不清楚。在本研究中,在人星形胶质细胞的纯化培养物中测定了MIP-1α的表达。通过逆转录聚合酶链反应(RT-PCR)测定人星形胶质细胞制剂中的MIP-1α mRNA水平,并通过酶联免疫吸附测定(ELISA)测定人星形胶质细胞分泌到培养上清液中的MIP-1α蛋白量。在未刺激的条件下,人星形胶质细胞不表达MIP-1α信息或蛋白,这表明人星形胶质细胞不组成性携带MIP-1α信息。在用白细胞介素-1β(IL-1β)处理后,人星形胶质细胞显示出MIP-1α的信息和蛋白表达增加,而其他免疫调节剂如干扰素-γ(IFN)-γ、肿瘤坏死因子-α(TNF-α)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、脂多糖或佛波酯(一种蛋白激酶C激活剂)在人星形胶质细胞中不诱导MIP-1α表达。

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