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Brain-specific chemokine FAM19A5 induces hypothalamic inflammation

Authors
Kang, DasolKim, Han RaeKim, Kwang KonKim, Dong HeeJeong, BoraJin, SunghoPark, Jeong WooSeong, Jae YoungLee, Byung Ju
Issue Date
19-3월-2020
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Tumor necrosis factor-alpha (TNF-alpha); Hypothalamic inflammation; Sickness responses; Anorexia; Hyperthermia; Proinflammatory cytokines
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.523, no.4, pp.829 - 834
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
523
Number
4
Start Page
829
End Page
834
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/57247
DOI
10.1016/j.bbrc.2019.12.119
ISSN
0006-291X
Abstract
The cytokine-like protein FAM19A5 is highly expressed in the brain, but little is known about its functions there. Here, we found that FAM19A5 was expressed in mouse hypothalamic cells expressing proopiomelanocortin (POMC) and neuropeptide Y (NPY)/agouti-related peptide (AgRP), and in the microglia. Tumor necrosis factor-alpha (TNF-alpha), which induces inflammatory sickness responses, greatly increased hypothalamic expression of FAM19A5. Knockdown of FAM19A5 expression resulted in decreased TNF-alpha-induced anorexia, body weight loss and TNF-alpha-induced expression of inflammatory factors. In contrast, intracerebroventricular administration of FAM19A5 induced anorexia, body weight loss and hyperthermia, together with increased expression of inflammatory factors. FAM19A5 injection also induced increases in c-fos activation and POMC mRNA level in hypothalamic POMC neurons. Together, these results suggest that FAM19A5 plays an important role in hypothalamic inflammatory responses. (C) 2020 Elsevier Inc. All rights reserved.
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