Currently published studies have implicated that microRNAs (miRNAs) including exosomes-encapsulated miRNAs play a critical role in rheumatoid arthritis (RA). Previously, we have found that exosomes-encapsulated miR-548a-3p was significantly decreased in serum samples from RA patients by miRNAs microarray analysis. However, little is known of the role of miR-548a-3p in the development and progression of RA. In this study, we aim to investigate the underlying molecular mechanisms of miR-548a-3p in RA, which will provide new insight into understanding the pathogenesis of RA and identifying novel therapeutics targets for this disease. As validated by quantitative real-time polymerase chain reaction (qRT-PCR), the expression of miR-548a-3p in serum exosomes and peripheral blood mononuclear cells (PBMCs) of RA patients (n = 76) was obviously down-regulated compared with healthy controls (n = 20). Serum exosomal miR-548a-3p was negatively associated with levels of CRP, RF, and ESR in serum of patients with RA. MiR-548a-3p could inhibit the proliferation and activation of pTHP-1 cells by regulating the TLR4/NF-κB signaling pathway. Accordingly, exosomes-delivered miR-548a-3p may be a critical factor predicting the disease activity of RA. MiR-548a-3p/TLR4/NF-κB axis can serve as promising targets for RA diagnosis and treatment.
Preeclampsia is a serious complication of pregnancy and leads to maternal hypertension and proteinuria. It remains a major health problem for mothers and babies across the world due to high maternal and fetal morbidity and mortality. Accumulated data have implicated the critical role of microRNA in preeclampsia. However, to date, the role of miR‐548c‐5p in preeclampsia remains vaguely understood. In this study, we first elucidate the role of miR‐548c‐5p and its underlying molecular mechanism in preeclampsia. Compared with healthy controls, miR‐548c‐5p was obviously downregulated in serum exosomes and placental mononuclear cells in patients with preeclampsia. Nonetheless, PTPRO was significantly upregulated and negatively associated with miR‐548c‐5p in placental mononuclear cells in patients with preeclampsia. PTPRO was a target of miR‐548c‐5p. PTPRO was downregulated in the miR‐548c‐5p‐overexpressed macrophages. In addition, miR‐548c‐5p could inhibit the proliferation and activation of LPS‐stimulated macrophages, as evidenced by decreased levels of inflammatory cytokines (IL‐12 and TNF‐α) and less nuclear translocation of pNF‐κB in pTHP1 cells. MiR‐548c‐5p acts as an anti‐inflammatory factor in preeclampsia. The axis of miR‐548c‐5p/PTPRO/NF‐κB may provide novel targets for the diagnosis and treatment of preeclampsia.
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