Oncotarget

Research Papers:

Macrophage migration inhibitory factor activates inflammatory responses of astrocytes through interaction with CD74 receptor

Yu Su, Yingjie Wang, Yue Zhou, Zhenjie Zhu, Qing Zhang, Xuejie Zhang, Wenjuan Wang, Xiaosong Gu, Aisong Guo and Yongjun Wang _

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Oncotarget. 2017; 8:2719-2730. https://doi.org/10.18632/oncotarget.13739

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Abstract

Yu Su1, Yingjie Wang1, Yue Zhou2, Zhenjie Zhu2, Qing Zhang1, Xuejie Zhang1, Wenjuan Wang1, Xiaosong Gu1, Aisong Guo2, Yongjun Wang1

1Key Laboratory of Neuroregeneration, Ministry of Education and Jiangsu Province, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China

2Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong 226001, PR China

Correspondence to:

Yongjun Wang, email: [email protected]

Aisong Guo, email: [email protected]

Keywords: MIF, spinal cord, astrocyte, inflammation, CD74

Received: September 06, 2016     Accepted: November 22, 2016     Published: December 01, 2016

ABSTRACT

Astrocytes, the major glial cell population of the central nervous system (CNS), play important physiological roles related to CNS homeostasis. Growing evidence demonstrates that astrocytes trigger innate immune responses under challenge of a variety of proinflammatory cytokines. Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine mainly secreted from monocytes/macrophages, is involved in inflammation-associated pathophysiology. Here, we displayed that expression of MIF significantly increased following spinal cord injury, in colocalization with microglia and astrocytes. MIF elicited inflammatory responses of astrocytes via activation of CD74 receptor and extracellular signal-related kinase (ERK) pathway. Transcriptome analysis revealed that inflammation-related factors cholesterol 25-hydroxylase (Ch25h) and phospholipase A2-IIA (Pla2g2a), downstream of MIF/CD74 axis, were potentially implicated in the mediating inflammatory response of astrocytes. Our results provided a new target for interference of CNS inflammation after insults.


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