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Publication
Beta cell secretion of miR-375 to HDL is inversely associated with insulin
secretion.
Authors Sedgeman LR, Beysen C, Ramirez Solano MA, Michell DL, Sheng Q, Zhao S, Turner S,
Linton MF, Vickers KC
Submitted By Submitted Externally on 4/8/2019
Status Published
Journal Scientific reports
Year 2019
Date Published 3/1/2019
Volume : Pages 9 : 3803
PubMed Reference 30846744
Abstract Extracellular microRNAs (miRNAs) are a new class of biomarkers for cellular
phenotypes and disease, and are bioactive signals within intercellular
communication networks. Previously, we reported that miRNAs are secreted from
macrophage to high-density lipoproteins (HDL) and delivered to recipient cells
to regulate gene expression. Despite the potential importance of HDL-miRNAs,
regulation of HDL-miRNA export from cells has not been fully studied. Here, we
report that pancreatic islets and beta cells abundantly export miR-375-3p to HDL
and this process is inhibited by cellular mechanisms that promote insulin
secretion. Small RNA sequencing and PCR approaches were used to quantify beta
cell miRNA export to HDL. Strikingly, high glucose conditions were found to
inhibit HDL-miR-375-3p export, which was dependent on extracellular calcium.
Likewise, stimulation of cAMP was found to repress HDL-miR-375-3p export.
Furthermore, we found that beta cell ATP-sensitive potassium channel (KATP)
channels are required for HDL-miRNA export as chemical inhibition (tolbutamide)
and global genetic knockout (Abcc8-/-) approaches inhibited HDL-miR-375-3p
export. This process is not likely associated with cholesterol flux, as
gain-of-function and loss-of-function studies for cholesterol transporters
failed to alter HDL-miR-375-3p export. In conclusion, results support that
pancreatic beta cells export miR-375-3p to HDL and this process is inversely
regulated to insulin secretion.





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