Both ERK and JNK are required for enhancement of MD-2 gene expression during differentiation of HL-60 cells
文献类型：期刊论文
| 作者 | Li, CL; Yu, YS; Wang, Y; Liu, L; Zhang, M; Sugano, SM; Wang, ZG; Chang, ZL |
| 刊名 | BIOLOGY OF THE CELL
 |
| 出版日期 | 2008 |
| 卷号 | 100期号:6页码:365-375 |
| 关键词 | c-Jun N-terminal kinase (JNK) Elk extracellular-signal-regulated kinase (ERK) MD-2 mRNA MD-2 promoter PMA |
| 通讯作者 | Chang, ZL (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.,chang_zong_liang@sibs.ac.cn |
| 英文摘要 | Background information. MD-2 is associated with the extracellular domain of TLR4 (Toll-like receptor 4) and augments TLR4-dependent LPS (lipopolysaccharide) responses in vitro. Our previous investigation found that PMA-induced HL-60 cell differentiation to macrophages is associated largely with TLR2 and CD14 and, to a much lesser extent, with TLR4. Results. We studied the MD-2 expression during differentiation of HL-60 cells induced by PMA. The results showed that PMA, but not VitD(3) (1 alpha,25-dihydroxy-vitamin D-3), strongly induces MD-2 gene expression by HL-60 cells in a time- and dose-dependent manner. Treatment with an MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitor (PD98059) and a JNK (c-Jun N-terminal kinase) inhibitor (SP600125) suppresses PMA-induced MD-2 gene expression, whereas impairment of p38 function by treatment with the inhibitor SB203580 has no effect on MD-2 mRNA. In order to reveal the possible molecular mechanism for such a regulation of MD-2 gene expression, we cloned and analysed the putative MD-2 gene promoter. Transient transfection of different deletion mutants demonstrated that the region - 185/-171 (5'-TCCTTTACAGGAAGT-3') of the MD-2 gene promoter is closely related to gene transcription in response to PMA. Additionally, the transcription factor Elk-1 has been found to bind this specific motif. Conclusions. These results suggest that ERK and JNK pathways are involved in PMA-mediated MD-2 gene expression during HL-60 cell differentiation, and the activation of the MEK/possible ERK/Elk signal pathway is the mechanism responsible for PMA-induced MD-2 gene expression in differentiated HL-60 cells. |
| 学科主题 | Cell Biology |
| 类目[WOS] | Cell Biology |
| 关键词[WOS] | PROTEIN-KINASE-C ; TOLL-LIKE RECEPTORS ; NF-KAPPA-B ; MURINE PERITONEAL-MACROPHAGES ; PMA-INDUCED DIFFERENTIATION ; MAP KINASES ; BACTERIAL LIPOPOLYSACCHARIDE ; IMMUNE-RESPONSE ; HUMAN MONOCYTES ; LEUKEMIA-CELLS |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000256406400004 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/1390]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Li, CL,Yu, YS,Wang, Y,et al. Both ERK and JNK are required for enhancement of MD-2 gene expression during differentiation of HL-60 cells[J]. BIOLOGY OF THE CELL,2008,100(6):365-375. |
| APA | Li, CL.,Yu, YS.,Wang, Y.,Liu, L.,Zhang, M.,...&Chang, ZL.(2008).Both ERK and JNK are required for enhancement of MD-2 gene expression during differentiation of HL-60 cells.BIOLOGY OF THE CELL,100(6),365-375. |
| MLA | Li, CL,et al."Both ERK and JNK are required for enhancement of MD-2 gene expression during differentiation of HL-60 cells".BIOLOGY OF THE CELL 100.6(2008):365-375. |
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