PMID- 32389166 OWN - NLM STAT- MEDLINE DCOM- 20200813 LR - 20200813 IS - 1007-8738 (Print) IS - 1007-8738 (Linking) VI - 36 IP - 3 DP - 2020 Mar TI - [CpG ODN synergistically promotes proliferation and migration of mouse RAW264.7 macrophages induced by lipopolysaccharide]. PG - 198-204 AB - Objective To investigate the effects of CpG oligodeoxynucleotide (CpG ODN) on the proliferation and migration of macrophages induced by lipopolysaccharide (LPS) and its mechanism. Methods In vitro inflammatory cell model was established by 1 mg/L LPS added into the culture medium of mouse RAW264.7 macrophages. CCK-8 assay was performed to assess the effect of CpG ODN (500 nmol/L) on the proliferation of macrophages induced by LPS; Transwell(TM) assay was used to measure the effect of CpG ODN (500 nmol/L) on the migration of macrophages induced by LPS. Western blot analysis was performed to detect the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK), c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases (ERK) and nuclear factor kappa-B subunits 65 (NF-kappaBp65). The specific inhibitors for p38MAPK (SB203580), JNK (SP600125), ERK (PD98059) and NF-kappaBp65 (BAY11-7082) were used to further explore the possible mechanism underlying the effects of CpG ODN. Real-time PCR was used to detect the role of CpG ODN in LPS-induced transcription of COX2 and MCP-1 in macrophages. Results CpG ODN synergistically enhanced the proliferation and migration of LPS-stimulated macrophages and promoted the transcription of COX2 and MCP-1. It also selectively enhanced the phosphorylation of JNK and ERK proteins in MAPK signaling pathway. To blockage JNK and ERK signaling pathways with its specific inhibitors dramatically inhibited the effects of CpG ODN. Conclusion CpG ODN can synergistically promote the proliferation and migration of LPS-stimulated macrophages through JNK and ERK pathway as well as the transcription of COX2 and MCP-1. FAU - Yang, Chunxiu AU - Yang C AD - Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou 510515, China. FAU - Qu, Yibai AU - Qu Y AD - Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou 510515, China. FAU - Yan, Zhengzheng AU - Yan Z AD - Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. *Corresponding author, E-mail: yzzaici888@163.com. LA - chi PT - Journal Article PL - China TA - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi JT - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology JID - 101139110 RN - 0 (Ccl2 protein, mouse) RN - 0 (Chemokine CCL2) RN - 0 (Lipopolysaccharides) RN - 0 (Oligodeoxyribonucleotides) RN - 0 (Rela protein, mouse) RN - 0 (Transcription Factor RelA) RN - EC 1.14.99.- (Ptgs2 protein, mouse) RN - EC 1.14.99.1 (Cyclooxygenase 2) RN - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) RN - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) SB - IM MH - Animals MH - *Cell Movement MH - *Cell Proliferation MH - Chemokine CCL2 MH - *CpG Islands MH - Cyclooxygenase 2 MH - JNK Mitogen-Activated Protein Kinases MH - Lipopolysaccharides MH - MAP Kinase Signaling System MH - Macrophages/*cytology/drug effects MH - Mice MH - Oligodeoxyribonucleotides/*pharmacology MH - RAW 264.7 Cells MH - Transcription Factor RelA MH - p38 Mitogen-Activated Protein Kinases EDAT- 2020/05/12 06:00 MHDA- 2020/08/14 06:00 CRDT- 2020/05/12 06:00 PHST- 2020/05/12 06:00 [entrez] PHST- 2020/05/12 06:00 [pubmed] PHST- 2020/08/14 06:00 [medline] PST - ppublish SO - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2020 Mar;36(3):198-204.