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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Neurotensin enhances nitric oxide generation via the JAK2-STAT1 pathway in murine macrophage Raw264.7 cells during costimulation with LPS and IFN gamma

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Title
Neurotensin enhances nitric oxide generation via the JAK2-STAT1 pathway in murine macrophage Raw264.7 cells during costimulation with LPS and IFN gamma
Author
Kim, HSYumkhaM, SChoi, Jang HyunLee, SHKim, THRyu, SHSuh, Pann-Ghill
Issue Date
2006-06
Publisher
CHURCHILL LIVINGSTONE
Citation
NEUROPEPTIDES, v.40, no.3, pp.221 - 229
Abstract
Neurotensin has been known to be implicated in immune function, but its molecular mechanisms remain largely unclear. In this study, we report that neurotensin increased the intracellular calcium levels of murine macrophage Raw264.7 cells, and that this calcium increase disappeared in the presence of either U73122, a PLC inhibitor, or SR48692, a neurotensin receptor antagonist. Also, the production of nitric oxide (NO) during costimulation with lipopolysaccharide (LPS) and interferon gamma (IFN gamma) was potentiated by exposure to neurotensin, whereas neurotensin itself had no ability to induce NO generation. The up-regulation of NO generation was correlated with the induction of inducible NO synthase (iNOS). In addition, the activities of janus activated kinase 2 (JAK2)-signal transducer and activated transcription 1 (STAT1) and the migration capacity of macrophage were increased as the result of costimulation of neurotensin with LPS and IFN gamma, and pretreatment of either U73122 or SR48692 attenuated these phenomenon. Moreover, the neurotensin-mediated enhancement of NO generation and migration were observed in the wild-type JAK2 transfected cells, but not in the dominant negative JAK2 transfected cells. Together, these results demonstrate that neurotensin can effect enhancement in LPS/IFN gamma-induced NO generation and migration capacity, via the JAK2-STAT1 pathway.
URI
https://scholarworks.unist.ac.kr/handle/201301/7266
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33747719879
DOI
10.1016/j.npep.2006.01.001
ISSN
0143-4179
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BIO_Journal Papers
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