한빛사 논문
Sung S. Choi1,†, Hong J. Lee1,†, Inja Lim2, Jun-ichi Satoh3, Seung U. Kim1,4,*
1 Medical Research Institute, Chung-Ang University College of Medicine, Seoul, Korea, 2 Department of Physiology, Chung-Ang University College of Medicine, Seoul, Korea, 3 Department of Bioinformatics and Molecular Neuropathology, Meiji Pharmaceutical University, Kiyose, Japan, 4 Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada
*Corresponding author
†These authors contributed equally to the work.
Abstract
Astrocytes play a key role in maintenance of neuronal functions in the central nervous system by producing various cytokines, chemokines, and growth factors, which act as a molecular coordinator of neuron-glia communication. At the site of neuroinflammation, astrocyte-derived cytokines and chemokines play both neuroprotective and neurotoxic roles in brain lesions of human neurological diseases. At present, the comprehensive profile of human astrocyte-derived cytokines and chemokines during inflammation remains to be fully characterized. We investigated the cytokine secretome profile of highly purified human astrocytes by using a protein microarray. Non-stimulated human astrocytes in culture expressed eight cytokines, including G-CSF, GM-CSF, GROα (CXCL1), IL-6, IL-8 (CXCL8), MCP-1 (CCL2), MIF and Serpin E1. Following stimulation with IL-1β and TNF-α, activated astrocytes newly produced IL-1β, IL-1ra, TNF-α, IP-10 (CXCL10), MIP-1α (CCL3) and RANTES (CCL5), in addition to the induction of sICAM-1 and complement component 5. Database search indicated that most of cytokines and chemokines produced by non-stimulated and activated astrocytes are direct targets of the transcription factor NF-kB. These results indicated that cultured human astrocytes express a distinct set of NF-kB-target cytokines and chemokines in resting and activated conditions, suggesting that the NF-kB signaling pathway differentially regulates gene expression of cytokines and chemokines in human astrocytes under physiological and inflammatory conditions.
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