4.5 Article

CC-CHEMOKINE LIGAND 18/PULMONARY ACTIVATION-REGULATED CHEMOKINE EXPRESSION IN THE CNS WITH SPECIAL REFERENCE TO TRAUMATIC BRAIN INJURIES AND NEOPLASTIC DISORDERS

期刊

NEUROSCIENCE
卷 165, 期 4, 页码 1233-1243

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2009.11.050

关键词

CC-chemokine; glia; microglia; macrophages; glioma; source; lesion

资金

  1. Shin-Kong WHS Memorial Hospital [SKH-TMU-95-15]
  2. National Science Council [NSC96-2320-B-016-010]

向作者/读者索取更多资源

Pulmonary activation-regulated chemokine (PARC) now designated CC-chemokine ligand 18 (CCL18) has been shown to play a significant role in the pathogenesis of various tissue injuries and diseases in a proinflammatory or immune suppressive way to limit or support the inflammation or disease. While much is known about the roles of CCL18/PARC in non-neural tissues, its expression in the CNS has remained largely unexplored and controversial. Using reverse transcription polymerase chain reaction (RT-PCR) and double immunohistochemical staining, we analyzed the expression of CCL18/PARC in the human brain with special reference to traumatic brain injuries and tumors. The RT-PCR analysis revealed the expression of CCL18/PARC mRNA both in the traumatic brain and glioma tissues examined. Immunoexpression of CCL18/PARC protein was consistently detected in all cases of traumatic brain injuries examined by immunohistochemical staining. Double immunofluorescence labeling has extended the study that CCL18/PARC positive cells were macrophages/microglia, astrocytes or neurons. The CCL18/PARC expression was localized in macrophage-like cells in two of eight glioblastoma tissues whose cancer cells were CCL18/PARC negative. Unexpectedly, CCL18/PARC mRNA weakly and constitutively expressed by glioblastoma cell line was upregulated after endotoxin stimulation. The present results indicated a significant production of CCL18/PARC in different CNS traumatic and neoplasm tissues by specific cellular elements expressing the chemokine. An anti-inflammatory mechanism jointly exerted by these cells via CCL18/PARC may be involved in the CNS immunity after traumatic injury and tumorigenesis. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.

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