The Estrogen-Induced miR-19 Downregulates Secretory Leucoprotease Inhibitor Expression in Monocytes.

摘要: Compared to females, males are more susceptible acute viral and other respiratory tract infections that display greater severity higher mortality. In contrast, females tend fare worse with chronic inflammatory diseases. Circulating 17β-estradiol (E2) is a female-specific factor may influence the progression of human lung Here we hypothesize E2 modulates response monocytes through microRNA (miRNA)-based modulation secretory leucoprotease inhibitor (SLPI), an antiprotease immunomodulatory effects. Monocytic cells were treated ± E2, differentially expressed miRNAs identified using PCR profiling. Cells transfected miRNA mimics or antimiRs SLPI mRNA protein levels quantified. Luciferase activity assay wildtype ΔmiR-19a/b-SLPI3′UTR reporter constructs chromatin immunoprecipitation on E2-treated performed. downregulated upregulated miR-19 expression in monocytes. Transfection premiR-19b reduced this effect was abrogated against miR-19b. miR-19b directly binds 3′UTR. The mechanism responsible for E2-mediated upregulation occurs via increased MIR17HG promoter mediated by c-MYC. Overall decreases monocytic cells, changes highlights potential estrogen modulate innate immune system.