Enhanced expression of TREM-1 in splenic cDCs in lupus prone mice and it was modulated by miRNA-150. (January 2017)

• Record Type: Journal Article
• Authors: Gao, Sheng; Yuan, Linbo; Wang, Yongyu; Hua, Chunyan
• Is Part Of: Molecular immunology. Volume 81(2017:Jan.)
• Page Start: 127
• Page End: 134
• Publication Date: 2017-01
• Subjects: SLE -- cDCs -- TREM-1 -- miRNA-150; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2016.12.006
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: We determined the activation status of cDCs and the expression of TREM-1 on cDCs in the context of lupus. We profiled the dysregulated miRNAs expression in splenocytes of lupus mice. We identified that miRNA-150 modulates TREM-1 expression. Abstract: Over activation of conventional dendritic cells (cDCs) contributes to the development of systemic lupus erythematosus (SLE). Triggering receptor expressed on myeloid cells 1 (TREM-1) is emerging as a potent amplifier of the inflammatory responses. We sought to determine the expression level of TREM-1 on cDCs in a mice model of SLE and to identify miRNA which could modulate TREM-1 expression. In the present study, TREM-1 expression in splenocytes and on cDCs was strongly up-regulated in vivo, and was enhanced with LPS stimulation in vitro . Blockade of TREM-1 signal impaired the TLR4-induced cytokines production. These indicated that TREM-1 potently amplified the function of TLR4 which enhanced the inflammation responses. A common set of dysregulated miRNAs (miRNA-98, -150 and -494) were identified in splenocytes of mice. Moreover, the results of bioinformatics and the immunoblotting, demonstrated that miRNA-150 inhibited the expression of TREM-1. Together, these data suggested that TREM-1 signaling pathway may be a therapeutic target to prevent the effects of the inflammatory cDCs in SLE and miRNA-150 serves as the important regulator.