Differences in Lipopolysaccharides-Induced Inflammatory Response Between Mouse Embryonic Fibroblasts and Bone Marrow-Derived Macrophages

被引:8
作者
Li, Yue [1 ]
Niu, Shixian [1 ]
Xi, Dalin [1 ]
Zhao, Shuqi [1 ]
Sun, Jiang [1 ]
Jiang, Yong [1 ]
Liu, Jinghua [1 ]
机构
[1] Southern Med Univ, Guangdong Prov Key Lab Prote, Sch Basic Med Sci, Guangzhou 510515, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
mouse embryonic fibroblasts; bone marrow-derived macrophages; lipopolysaccharide; inflammatory cytokines; intracellular signal pathways; P38; MAPK; PROLIFERATION; ACTIVATION; EXPRESSION; CYTOKINES;
D O I
10.1089/jir.2018.0167
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mouse embryonic fibroblasts (MEFs) are commonly used in research on the molecular mechanism(s) of inflammation because of its good response to inflammatory stimuli. However, the difference in inflammatory reaction between MEFs and macrophages, a classical inflammatory cell type, has not been identified. In this study, we report that both mRNA and protein levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in MEFs upon lipopolysaccharides (LPS) stimulation were significantly lower than those in bone marrow-derived macrophages (BMDMs). MAPK, NF-kappa B, and IRF3 pathways control the expression and production of inflammatory activated in LPS-stimulated MEFs, but showed different activation patterns in comparison with LPS-stimulated BMDMs. Upon LPS stimulation, activation of the MAPK pathway was slow and remarkably weaker in MEFs than that in BMDMs, whereas more pronounced activation of both NF-kappa B and IRF3 pathways was observed in MEFs compared to BMDMs. This difference in the activation of MAPK, NF-kappa B, and IRF3 pathways may result in different production of IL-6 and TNF-alpha between MEFs and BMDMs. We further revealed that substantial differences in more additional inflammatory response-related cytokines exist between LPS-stimulated MEFs and BMDMs. In conclusion, MEFs exhibit good responsiveness to LPS as a target cell for inflammation-related research. However, MEFs cannot replace macrophages because of substantial differences in their inflammatory reactivity.
引用
收藏
页码:375 / 382
页数:8
相关论文
共 30 条
  • [1] FLICE-like inhibitory protein (FLIP) protects against apoptosis and suppresses NF-K13 activation induced by bacterial lipopolysaccharide
    Bannerman, DD
    Eiting, KT
    Winn, RK
    Harlan, JM
    [J]. AMERICAN JOURNAL OF PATHOLOGY, 2004, 165 (04) : 1423 - 1431
  • [2] Variation in Antagonism of the Interferon Response to Rotavirus NSP1 Results in Differential Infectivity in Mouse Embryonic Fibroblasts
    Feng, N.
    Sen, A.
    Nguyen, H.
    Vo, P.
    Hoshino, Y.
    Deal, E. M.
    Greenberg, H. B.
    [J]. JOURNAL OF VIROLOGY, 2009, 83 (14) : 6987 - 6994
  • [3] Garfield AS, 2010, METHODS MOL BIOL, V633, P19, DOI 10.1007/978-1-59745-019-5_2
  • [4] Alternative Activation of Macrophages: Mechanism and Functions
    Gordon, Siamon
    Martinez, Fernando O.
    [J]. IMMUNITY, 2010, 32 (05) : 593 - 604
  • [5] Modelling the interactions between TLR4 and IFNβ pathways
    Gunel, Aylin
    [J]. JOURNAL OF THEORETICAL BIOLOGY, 2012, 307 : 137 - 148
  • [6] Inflammation and Atherosclerosis: A Review of the Role of Interleukin-6 in the Development of Atherosclerosis and the Potential for Targeted Drug Therapy
    Hartman, Joshua
    Frishman, William H.
    [J]. CARDIOLOGY IN REVIEW, 2014, 22 (03) : 147 - 151
  • [7] Multiple activation mechanisms of p38α mitogen-activated protein kinase
    Kang, Young Jun
    Seit-Nebi, Alim
    Davis, Roger J.
    Han, Jiahuai
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (36) : 26225 - 26234
  • [8] Akt1 mediates the posterior Hoxc gene expression through epigenetic modifications in mouse embryonic fibroblasts
    Kong, Kyoung-Ah
    Lee, Ji-Yeon
    Oh, Ji Hoon
    Lee, Youra
    Kim, Myoung Hee
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, 2014, 1839 (09): : 793 - 799
  • [9] Lee Migi, 2017, J Biomol Tech, V28, P67, DOI 10.7171/jbt.17-2802-003
  • [10] β-Arrestin 2 Negatively Regulates Toll-like Receptor 4 (TLR4)-triggered Inflammatory Signaling via Targeting p38 MAPK and Interleukin 10
    Li, Hui
    Hu, Dan
    Fan, Huimin
    Zhang, Ying
    LeSage, Gene D.
    Caudle, Yi
    Stuart, Charles
    Liu, Zhongmin
    Yin, Deling
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2014, 289 (33) : 23075 - 23085