Inhibition by the JAK/STAT pathway of IFNγ- and LPS-stimulated nitric oxide synthase induction in vascular smooth muscle cells
Inhibition by the JAK/STAT pathway of IFNγ- and LPS-stimulated nitric oxide synthase induction in vascular smooth muscle cells
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DOI：
10.1006/bbrc.1998.9678
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发表时间：
1998-11-18
影响因子：
3.1
通讯作者：
Venema, RC
中科院分区：
文献类型：
--
作者：
Marrero, MB;Venema, VJ;Venema, RC
诱导型一氧化氮合酶（iNOS）是由细胞因子和脂多糖（LPS）诱导的多种细胞类型。细胞因子信号转导被认为主要通过JAK/STAT通路介导。因此，我们研究了JAK2特异性抑制剂（JAK2的反义寡核苷酸）和电穿孔中和抗stat1和抗stat3抗体对IFN γ和lps刺激的血管平滑肌细胞iNOS诱导的影响。出乎意料的是，我们发现JAK/STAT通路抑制IFN γ和lps刺激的这些细胞中的iNOS诱导。相反，JAK/STAT通路似乎在RAW 264.7巨噬细胞的iNOS诱导中起积极作用。(C) 1998学术出版社。
Inducible nitric oxide synthase (iNOS) is induced in many cell types by cytokines and lipopolysaccharide (LPS). Cytokine signal transduction is believed to be mediated primarily through the JAK/STAT pathway. We therefore examined the effects of a JAK2-specific inhibitor, an antisense oligonucleotide to JAK2, and electroporation of neutralizing anti-STAT1 and anti-STAT3 antibodies on IFN gamma- and LPS-stimulated induction of iNOS in vascular smooth muscle cells. Unexpectedly, we found that the JAK/STAT pathway suppresses IFN gamma- and LPS-stimulated iNOS induction in these cells. In contrast, the JAK/STAT pathway appears to have a positive role in iNOS induction in RAW 264.7 macrophages. (C) 1998 Academic Press.