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• W2990431414 abstract "This study was designed to evaluate the roles of microRNAs (miRNAs) in slow transit constipation (STC).All human tissue samples were from the muscularis externa of the colon. Expression of 372 miRNAs was examined in a discovery cohort of four patients with STC versus three age/sex-matched controls by a quantitative PCR array. Upregulated miRNAs were examined by quantitative reverse transcription qPCR (RT-qPCR) in a validation cohort of seven patients with STC and age/sex-matched controls. The effect of a highly differentially expressed miRNA on a custom human smooth muscle cell line was examined in vitro by RT-qPCR, electrophysiology, traction force microscopy, and ex vivo by lentiviral transduction in rat muscularis externa organotypic cultures.The expression of 13 miRNAs was increased in STC samples. Of those miRNAs, four were predicted to target SCN5A, the gene that encodes the Na+ channel NaV1.5. The expression of SCN5A mRNA was decreased in STC samples. Let-7f significantly decreased Na+ current density in vitro in human smooth muscle cells. In rat muscularis externa organotypic cultures, overexpression of let-7f resulted in reduced frequency and amplitude of contraction.A small group of miRNAs is upregulated in STC, and many of these miRNAs target the SCN5A-encoded Na+ channel NaV1.5. Within this set, a novel NaV1.5 regulator, let-7f, resulted in decreased NaV1.5 expression, current density and reduced motility of GI smooth muscle. These results suggest NaV1.5 and miRNAs as novel diagnostic and potential therapeutic targets in STC." @default.
• W2990431414 created "2019-12-05" @default.
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• W2990431414 date "2019-11-22" @default.
• W2990431414 modified "2023-10-11" @default.
• W2990431414 title "microRNA overexpression in slow transit constipation leads to reduced Na_V1.5 current and altered smooth muscle contractility" @default.
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• W2990431414 doi "https://doi.org/10.1136/gutjnl-2019-318747" @default.
• W2990431414 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7147984" @default.

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