title: Enhanced expression of TREM-1 in splenic cDCs in lupus prone mice and it was modulated by miRNA-150.
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.
authors.affiliation: School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Gao
authors.affiliation: School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
authors.forename: Linbo
authors.initials: L
authors.lastname: Yuan
authors.affiliation: School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
authors.forename: Yongyu
authors.initials: Y
authors.lastname: Wang
authors.affiliation: School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China. Electronic address: florshine@163.com.
authors.forename: Chunyan
authors.initials: C
authors.lastname: Hua
mesh_terms: D000818:Animals; D015153:Blotting, Western; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000235:genetics / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D035683:MicroRNAs / Q000276:immunology*; D016133:Polymerase Chain Reaction; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000276:immunology; D013154:Spleen / Q000276:immunology; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
chemical_list: D008562:Membrane Glycoproteins; D035683:MicroRNAs; C529101:Mirn150 microRNA, mouse; D011971:Receptors, Immunologic; C517262:TREM1 protein, mouse; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
keywords: SLE; TREM-1; cDCs; miRNA-150