Estradiol inhibits fMLP-induced neutrophil migration and superoxide production by upregulating MKP-2 and dephosphorylating ERK
文献类型:期刊论文
作者 | Zhang, Ping1; Wan, Dapeng1; Su, Hao1; Wang, Zhaodong1; Hou, Ruixing1,4; Fu, Yi2; Rui, Huajuan3; Ju, Jihui4; Jin, Qianheng4; Le, Yingying5 |
刊名 | INTERNATIONAL IMMUNOPHARMACOLOGY
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出版日期 | 2019 |
卷号 | 75期号:-页码:105787 |
关键词 | Estradiol Neutrophil Chemotaxis Reactive oxygen species MKP-2 ERK |
ISSN号 | 1567-5769 |
DOI | 10.1016/j.intimp.2019.105787 |
文献子类 | Article |
英文摘要 | Estrogen has been reported to inhibit neutrophil infiltration related inflammation and suppress neutrophils migration in vitro, but the underlying mechanism is not fully understood. By using HL-60 differentiated neutrophil-like cells (dHL-60) and human neutrophils, we examined the effect of 17-beta estradiol (E-2) on cell migration and superoxide production in response to chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLP) and explored the mechanisms involved. We found that fMLP significantly induced dHL-60 cell and neutrophil migration and superoxide production, which was inhibited by ERK inhibitor PD98059. E-2 significantly inhibited fMLP-induced dHL-60 cell and neutrophil migration and superoxide production at both physiological and pharmacological concentrations. Mechanistic studies showed that pretreatment of these cells with E-2 rapidly elevated the protein level of mitogen-activated protein kinase phosphatase 2 (MKP-2) and inhibited fMLP-induced ERK phosphorylation. Pretreatment of these cells with estrogen receptor (ER) antagonist ICI 182780 reversed the inhibition of fMP-induced cell migration and superoxide production, and the induction of MKP-2 expression and the suppression of fMP-induced ERK phosphorylation by E-2. However, pretreatment of cells with G-protein coupled ER antagonist G15 had no such effect. Collectively, these results demonstrate that fMLP stimulates neutrophil chemotaxis and superoxide production through activating ERK, and indicate that ER-mediated upregulation of MKP-2 may dephosphorylate ERK and contribute to the inhibitory effect of E-2 on neutrophil activation by fMLP. Our study reveals new mechanisms involved in the anti-inflammatory activity of estrogen. |
学科主题 | Biotechnology & Applied Microbiology ; Oncology |
WOS关键词 | ACTIVATED PROTEIN-KINASE ; ISCHEMIA-REPERFUSION ; POSTTRANSLATIONAL REGULATION ; PHOSPHATASE-2 MKP-2 ; OXIDATIVE BURST ; ESTROGEN ACTION ; SEX-HORMONES ; HL-60 CELLS ; TNF-ALPHA ; RECEPTOR |
语种 | 英语 |
CSCD记录号 | CSCD:31401382 |
WOS记录号 | WOS:000488998800063 |
出版者 | ELSEVIER |
版本 | 出版稿 |
源URL | [http://202.127.25.144/handle/331004/1217] ![]() |
专题 | 中国科学院上海生命科学研究院营养科学研究所 |
作者单位 | 1.Soochow Univ, Ruihua Affiliated Hosp, Inst Hand Surg, Suzhou 215100, Jiangsu, Peoples R China; 2.Soochow Univ, Sch Biol & Basic Med Sci, Dept Human Anat Histol & Embryol, Suzhou 215007, Jiangsu, Peoples R China; 3.Soochow Univ, Ruihua Affiliated Hosp, Dept Clin Lab, Suzhou 215100, Jiangsu, Peoples R China; 4.Soochow Univ, Ruihua Affiliated Hosp, Dept Hand Surg, Suzhou 215100, Jiangsu, Peoples R China; 5.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Nutr & Hlth,CAS Key Lab Nutr Metab, Shanghai, Peoples R China, |
推荐引用方式 GB/T 7714 | Zhang, Ping,Wan, Dapeng,Su, Hao,et al. Estradiol inhibits fMLP-induced neutrophil migration and superoxide production by upregulating MKP-2 and dephosphorylating ERK[J]. INTERNATIONAL IMMUNOPHARMACOLOGY,2019,75(-):105787. |
APA | Zhang, Ping.,Wan, Dapeng.,Su, Hao.,Wang, Zhaodong.,Hou, Ruixing.,...&,.(2019).Estradiol inhibits fMLP-induced neutrophil migration and superoxide production by upregulating MKP-2 and dephosphorylating ERK.INTERNATIONAL IMMUNOPHARMACOLOGY,75(-),105787. |
MLA | Zhang, Ping,et al."Estradiol inhibits fMLP-induced neutrophil migration and superoxide production by upregulating MKP-2 and dephosphorylating ERK".INTERNATIONAL IMMUNOPHARMACOLOGY 75.-(2019):105787. |
入库方式: OAI收割
来源:上海营养与健康研究所
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