Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase.
Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase.
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DOI：
10.1016/j.amjsurg.2009.12.004
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发表时间：
2010-08
影响因子：
3
通讯作者：
Samuel, Isaac
中科院分区：
文献类型：
--
作者：
Williard, Deborah E.;Twait, Erik;Yuan, Zuobiao;Carter, A. Brent;Samuel, Isaac
有丝分裂原活化蛋白（MAP）激酶和核因子κ-B（NF-κB）参与急性胰腺炎发病的早期阶段。我们在分离的腺泡细胞中研究了p38 MAP激酶与NF-κB B的关系。在用含有仅由NF-κB驱动的荧光素酶启动子的腺病毒载体和含有显性阴性（DN）形式的p38的腺病毒载体（对照中为空载体）感染后，用激动剂刺激分离的啮齿动物腺泡细胞。初步免疫印迹证实，激动剂刺激的p38激活腺泡细胞基本上减弱DN p38过表达。天然CCK-A受体或TNF-α受体的刺激促进了空载体感染细胞中NF-κ B依赖性基因转录的显著增加，而DN p38的过度表达显著消除了NF-κ B依赖性荧光素酶活性。这些发现支持我们的假设，即p38参与胰腺外分泌细胞中促炎性核转录因子如NF-κB的激活。
Mitogen activated protein (MAP) kinases and nuclear factor kappa-B (NF-κB) are implicated in early stages of acute pancreatitis pathogenesis. We investigated the relationship between the p38 MAP kinase and NF-κB in isolated acinar cells. Isolated rodent acinar cells were stimulated with agonists after infection with an adenovector containing a luciferase promotor driven only by NF-κB and an adenovector containing the dominant negative (DN) form of p38 (empty vector in controls). Initial immunoblots confirmed that the agonist stimulated p38 activation in acinar cells was substantially attenuated by DN p38 over expression. Stimulation of native CCK-A receptors or TNF-α receptors promoted a significant increase in NF-κB-dependent gene transcription in cells infected with the empty vector, while over expression of DN p38 significantly abrogated NF-κB-dependent luciferase activity. These findings support our hypothesis that p38 is involved in the activation of proinflammatory nuclear transcription factors such as NF-κB in pancreatic exocrine cells.
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DOI：
10.1152/ajpgi.00500.2006
发表时间：
2007-06-01
影响因子：
4.5
作者：
Husain, Sohail Z.;Grant, Wayne M.;Shah, Ahsan U.
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影响因子：
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作者：
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作者：
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影响因子：
4.8
作者：
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通讯作者：
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影响因子：
4.8
作者：
Morel, C;Ibarz, G;Martinez, J
通讯作者：
Martinez, J