Fractalkine stimulates cell growth and increases its expression via NF-?B pathway in RA-FLS

被引:24
|
作者
Guo, Xinghua [1 ]
Pan, Yunfeng [1 ]
Xiao, Chuyin [1 ]
Wu, Yuqiong [1 ]
Cai, Daozhang [2 ]
Gu, Jieruo [1 ]
机构
[1] Sun Yat Sen Univ, Hosp 3, Dept Rheumatol, Guangzhou 510630, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Hosp 3, Dept Orthopaed, Guangzhou 510630, Guangdong, Peoples R China
关键词
cell proliferation; CX3CL1; fibroblast-like synoviocyte; NF-?B; rheumatoid arthritis; FIBROBLAST-LIKE SYNOVIOCYTES; RHEUMATOID-ARTHRITIS; KAPPA-B; JOINT DESTRUCTION; TNF-ALPHA; PROLIFERATION; ACTIVATION; RESPONSES; PROTEIN; KINASE;
D O I
10.1111/j.1756-185X.2012.01721.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background After the onset of rheumatoid arthritis (RA), fibroblast-like synoviocytes (RA-FLS) which are specialized types of fibroblasts, become tumor-like, keeping their ability to increase proliferation and invasion. The mechanism of their tumor-like growth is unclear. Fractalkine (FKN), also called CX3CL1, plays an important role in the proliferation of cells. FKN may stimulate the proliferation of RA-FLS and the by nuclear factor ?B (NF-?B) pathway may be one of the steps in this process. Objective To investigate whether FKN can stimulate cell growth and increase its expression in RA-FLS, and the relationship between the NF-?B pathway and the function of FKN. Methods FLS were isolated from primary synovial tissue obtained from three patients with RA who had undergone total joint replacement surgery or synovectomy in the Third Hospital Affiliated to Sun Yat-sen University from February 2009 to January 2010. FKN was used in different concentrations to stimulate RA-FLS with or without NF-?B pathway blocker (PDTC), and to test the proliferation of FLS after 24 similar to h by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. RA-FLS was treated with 100ng/mL FKN or 100 mu M PDTC for different periods, and messenger RNA (mRNA) expression of FKN and CX3CR1 in RA-FLS was detected by reverse transcription polymerase chain reaction. We then tested the protein expression of NF-?Bp65 in the cytoplasm and nucleus, respectively by Western blotting after treating the RA-FLS with 100ng/mL FKN for different time periods. Results FKN stimulated cell growth in RA-FLS at the concentration of 50 or 100ng/mL (P=0.005 and P=0.022, respectively). NF-?B pathway blocker inhibited FKN, promoting proliferation of RA-FLS. RA-FLS could express FKN and CX3CR1 mRNA in vitro. FKN up-regulated FKN expression after 18-h treatment (P similar to=similar to 0.012). PDTC disturbed the expression of FKN mRNA after 1618 similar to h treatment (P similar to=similar to 0.001 and P similar to <similar to 0.001, respectively). After stimulation with FKN for 1 similar to h, the expression of NF-?Bp65 in cytoplasm began to decrease (P similar to=similar to 0.010), and the expression of NF-?Bp65 in the nucleus began to increase after 2 similar to h (P similar to=similar to 0.011). Conclusion These results suggest that FKN stimulates cells growth in RA-FLS and NF-?B pathway blocker inhibits FKN, promoting proliferation of RA-FLS. FKN induced activation of NF-?B activity. FKN up-regulates FKN mRNA expression in RA-FLS via the NF-?B pathway.
引用
收藏
页码:322 / 329
页数:8
相关论文
共 50 条
  • [1] Clock Gene Bmal1 Contributes to Inflammation via Phosphorylation of NF-κB/p65 in RA-FLS
    Tsukamoto, Hikari
    Kaneshiro, Kenta
    Yoshida, Kohsuke
    Tateishi, Koji
    Terashima, Yasuhiro
    Shibanuma, Nao
    Sakai, Yoshitada
    Hashiramoto, Akira
    ARTHRITIS & RHEUMATOLOGY, 2024, 76 : 5265 - 5266
  • [2] Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway
    Guan, Yin
    Zhao, Xiaoqian
    Liu, Weiwei
    Wang, Yue
    JOURNAL OF ORTHOPAEDIC SURGERY AND RESEARCH, 2020, 15 (01)
  • [3] Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway
    Yin Guan
    Xiaoqian Zhao
    Weiwei Liu
    Yue Wang
    Journal of Orthopaedic Surgery and Research, 15
  • [4] Heilaohuacid G, a new triterpenoid from Kadsura coccinea inhibits proliferation, induces apoptosis, and ameliorates inflammation in RA-FLS and RAW 264.7 cells via suppressing NF-κB pathway
    Yang, Yu-pei
    Jian, Yu-qing
    Liu, Yong-bei
    Xie, Qing-ling
    Yu, Huang-he
    Wang, Bin
    Li, Bin
    Peng, Cai-yun
    Wang, Wei
    PHYTOTHERAPY RESEARCH, 2022, 36 (10) : 3900 - 3910
  • [5] Clock Gene Bmal1 Promotes Transcriptional Activity of NF-κB to Regulate Production of Inflammatory Mediators in RA-FLS
    Tsukamoto, Hikari
    Kaneshiro, Kenta
    Yoshida, Kohsuke
    Tateishi, Koji
    Terashima, Yasuhiro
    Shibanuma, Nao
    Sakai, Yoshitada
    Hashiramoto, Akira
    ARTHRITIS & RHEUMATOLOGY, 2023, 75 : 15 - 17
  • [6] IL-34 regulates MAPKs, PI3K/Akt, JAK and NF-?B pathways and induces the expression of inflammatory factors in RA-FLS
    Yang, H.
    Luo, Y.
    Lai, X.
    CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, 2022, 40 (09) : 1779 - 1788
  • [7] DOWN-REGULATED PGC-1β COULD INHIBIT RA-FLS INDUCED OSTEOCLASTOGENESIS AND BONE RESORPTION BY SUPPRESSION OF NF-κB ACTIVATION
    Liang, J. -J.
    Zhou, J. -J.
    Ma, J. -D.
    Zheng, D. -H.
    Mo, Y. -Q.
    Wei, X. -N.
    Dai, L.
    ANNALS OF THE RHEUMATIC DISEASES, 2015, 74 : 661 - 662
  • [8] PMPs通过CXCR2/Erk/NF-κB通路影响RA-FLS中RANKL和OPG表达的研究
    杨洁
    王雯雯
    张晨
    邓子靖
    周玮
    沈维干
    张育
    扬州大学学报(农业与生命科学版), 2021, 42 (01) : 41 - 46+57
  • [9] Nox 2 stimulates muscle differentiation via NF-κB/iNOS pathway
    Piao, YJ
    Seo, YH
    Hong, F
    Kim, JH
    Kim, YJ
    Kang, MH
    Kim, BS
    Jo, SA
    Jo, I
    Jue, DM
    Kang, I
    Ha, J
    Kim, SS
    FREE RADICAL BIOLOGY AND MEDICINE, 2005, 38 (08) : 989 - 1001
  • [10] MicroRNA-181b Stimulates Inflammation via NF-κB Signaling Pathway in Vitro
    Wang, Y. Z.
    Mao, G. X.
    Lv, Y. D.
    Huang, Q. D.
    Wang, G. F.
    JOURNAL OF THE AMERICAN GERIATRICS SOCIETY, 2014, 62 : S394 - S394