國家衛生研究院 NHRI:Item 3990099045/11116
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    題名: Monosodium urate crystals induced ICAM-1 expression and cell–cell adhesion in renal mesangial cells: Implications for the pathogenesis of gouty nephropathy
    作者: Luo, SF;Chin, CY;Ho, LJ;Tseng, WY;Kuo, CF;Lai, JH
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: Background: Renal disease is prevalent in gouty patients and monosodium urate (MSU) crystal deposition in the kidney can be detected in some gouty nephropathy patients. MSU crystals can induce inflammatory events, we investigated the MSU-induced expression of intercellular adhesion molecule (ICAM)-1 on human renal mesangial cells (HRMCs) and the involved signal transduction mechanisms. Methods: The HRMCs cell line was purchased from ScienCell Research Laboratories. MSU crystals were made by dissolving uric acid in sodium hydroxide (NaOH) solution. The involvement of MAPKs, apoptosis-associated speck-like protein containing a CARD domain (ASC), and Toll-like receptor (TLR) was investigated using pharmacological inhibitors, transfection with short hairpin RNA (shRNA), or monoclonal antibodies. Protein expression was evaluated by Western blotting. The functional activity of ICAM-1 was evaluated with cell–cell adhesion assay and immunofluorescence analysis. Results: MSU stimulation increased expression of ICAM-1 and adhesion between HRMCs and human monocytic THP-1 cells. The interaction between HRMCs and THP-1 was suppressed by ICAM-1 neutralizing antibodies. MSU stimulation induced activation of mitogen-activated protein kinases, including c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK), but only p38 was responsible for MSU-induced expression of ICAM-1 and cell–cell adhesion. ASC also play a role in MSU-induced effects. Pretreatment with monoclonal antibodies against toll-like receptor (TLR)2 or TLR4 reduced MSU-induced ICAM-1 expression, cell–cell adhesion, p38 phosphorylation but the reduction of ASC activation is insignificant. Conclusion: The MSU induced ICAM-1 expression on HRMCs and cell–cell adhesion involved TLR2/4-p38-ICAM1 pathway and TLR2/4 independent ASC-p38-ICAM1 axis. These findings might partly explain the mechanisms underlying gouty nephropathy.
    日期: 2020-02
    關聯: Journal of Microbiology, Immunology and Infection. 2020 Feb;53(1):23-32.
    Link to: http://dx.doi.org/10.1016/j.jmii.2017.12.004
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1684-1182&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000516797400003
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85045312703
    顯示於類別:[何令君] 期刊論文

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