2 research outputs found
Melatonin Maintains Homeostasis and Potentiates the Anti-inflammatory Response in Staphylococcus aureus-Induced Mastitis through microRNA-16b/YAP1
Staphylococcus aureus is
a highly
infectious pathogen and is a considerable threat to food hygiene and
safety. Although melatonin is thought to exert an ameliorative effect
on bovine mastitis, the regulatory mechanisms are unclear. In this
study, we first verified the therapeutic effect of melatonin against S. aureus in vitro and in vivo, a screening of differentially
expressed miRNAs and mRNAs among the blank, and S.
aureus and melatonin + S. aureus groups by high-throughput sequencing identified miR-16b and YAP1, which exhibited 1.95-fold upregulated and 1.05-fold
downregulated expression, respectively. Moreover, epigenetic studies
showed that S. aureus inhibited miR-16b
expression by methylation (increased DNMT1 expression). Additionally,
the DNMT1 expression level was significantly decreased
by melatonin treatment, which might indicate that the inhibition of DNMT1 by melatonin reduces the effect of S. aureus on miR-16b. The flow cytometry, scanning
and transmission electron microscopy, EdU assay, and cell morphology
results indicated that miR-16b in bovine mammary epithelial cells
(in vitro) and in mice (in vivo) can modulate the maintenance of homeostasis
and potentiate the anti-inflammatory response. In addition, YAP1 was demonstrated to be the target gene of miR-16b through
quantitative real-time polymerase chain reaction, western blot, RNA
immunoprecipitation, and functional assays. This study indicates that
melatonin inhibits S. aureus-induced
inflammation via microRNA-16b/YAP1-mediated regulation,
and these findings might provide a new strategy for the prevention
of bovine mastitis, facilitating further studies good of zoonotic
diseases caused by S. aureus infection
Melatonin Maintains Homeostasis and Potentiates the Anti-inflammatory Response in Staphylococcus aureus-Induced Mastitis through microRNA-16b/YAP1
Staphylococcus aureus is
a highly
infectious pathogen and is a considerable threat to food hygiene and
safety. Although melatonin is thought to exert an ameliorative effect
on bovine mastitis, the regulatory mechanisms are unclear. In this
study, we first verified the therapeutic effect of melatonin against S. aureus in vitro and in vivo, a screening of differentially
expressed miRNAs and mRNAs among the blank, and S.
aureus and melatonin + S. aureus groups by high-throughput sequencing identified miR-16b and YAP1, which exhibited 1.95-fold upregulated and 1.05-fold
downregulated expression, respectively. Moreover, epigenetic studies
showed that S. aureus inhibited miR-16b
expression by methylation (increased DNMT1 expression). Additionally,
the DNMT1 expression level was significantly decreased
by melatonin treatment, which might indicate that the inhibition of DNMT1 by melatonin reduces the effect of S. aureus on miR-16b. The flow cytometry, scanning
and transmission electron microscopy, EdU assay, and cell morphology
results indicated that miR-16b in bovine mammary epithelial cells
(in vitro) and in mice (in vivo) can modulate the maintenance of homeostasis
and potentiate the anti-inflammatory response. In addition, YAP1 was demonstrated to be the target gene of miR-16b through
quantitative real-time polymerase chain reaction, western blot, RNA
immunoprecipitation, and functional assays. This study indicates that
melatonin inhibits S. aureus-induced
inflammation via microRNA-16b/YAP1-mediated regulation,
and these findings might provide a new strategy for the prevention
of bovine mastitis, facilitating further studies good of zoonotic
diseases caused by S. aureus infection