Regulation of cytokine-induced prostanoid and nitric oxide synthesis by extracellular signal–regulated kinase 1/2 in lung epithelial cells.
Regulation of cytokine-induced prostanoid and nitric oxide synthesis by extracellular signal–regulated kinase 1/2 in lung epithelial cells.
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DOI：
10.3109/01902148.2010.491891
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发表时间：
2010-11
影响因子：
1.7
通讯作者：
Dwyer-Nield LD
中科院分区：
文献类型：
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作者：
Rice PL;Barrett BS;Fritz JM;Srebernak MC;Kisley LR;Malkinson AM;Dwyer-Nield LD
The inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interferon gamma (IFNγ), stimulate production of the inflammatory mediators prostaglandin (PG) E2, PGI2, and nitric oxide (NO) in cultured lung epithelial cells. Pre-treatment of these cells with the selective MEK1/2 inhibitor, U0126, blocked ERK1/2 activation and inhibited cytokine-induced production of these inflammatory mediators. Primary bronchiolar epithelial Clara cells treated with TNFα and IFNγ also produced increased PGE2, PGI2, and NO, and PG and NO production was decreased by MEK inhibition. U0126 differentially affected COX-1, COX-2 and iNOS expression in cell lines, however, suggesting that MEK1/2 regulates prostanoid and NO production by means other than inducing their biosynthetic enzymes. Functionally, inhibition of MEK1/2 caused G1 cell cycle arrest and decreased cyclin D1 expression, but these effects were not related to decreased prostanoid production. These results indicate separate pro-inflammatory and proliferative roles for ERK1/2 in lung epithelial cells. During lung tumor formation in vivo, ERK1/2 phosphorylation increased as lung tumors progressed. Since tumor-derived cells were more sensitive than non-tumorigenic cells to the anti-proliferative effects of U0126, MEK1/2 inhibition may serve as an attractive chemotherapeutic target.
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影响因子：
254.7
作者：
Jemal, Ahmedin;Siegel, Rebecca;Thun, Michael J.
通讯作者：
Thun, Michael J.
有效使用 PI3K 和 MEK 抑制剂治疗突变型 Kras G12D 和 PIK3CA H1047R 小鼠肺癌。
影响因子：
82.9
作者：
通讯作者：
--
影响因子：
15.9
作者：
Asano, K;Nakamura, H;Drazen, JM
通讯作者：
Drazen, JM
影响因子：
3.6
作者：
Ballaz, Santiago;Mulshine, James L
通讯作者：
Mulshine, James L
影响因子：
7.3
作者：
Belvisi, MG;Saunders, MA;Mitchell, JA
通讯作者：
Mitchell, JA