ArticleScientific reports2016
Neurotensin-induced miR-133α expression regulates neurotensin receptor 1 recycling through its downstream target aftiphilin.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Exosomes Derived from hucMSCs Primed with IFN-γ Suppress the NF-κB Signal Pathway in LPS-Induced ALI by Modulating the miR-199b-5p/AFTPH Axis.Cell biochemistry and biophysics · 2024Article
- NTSR1 glycosylation and MMP dependent cleavage generate three distinct forms of the protein.Scientific reports · 2023Article
- Review
- Aftiphilin Regulation of Myosin Light Chain Kinase Activity Promotes Actin Dynamics and Intestinal Epithelial Barrier Function.Frontiers in gastroenterology (Lausanne, Switzerland) · 2022Article
- The microRNA-204-5p inhibits APJ signalling and confers resistance to cardiac hypertrophy and dysfunction.Clinical and translational medicine · 2022Article
- miRNA-Based Potential Biomarkers and New Molecular Insights in Ulcerative Colitis.Frontiers in pharmacology · 2021Review
- Expression profiles and prognostic significance of AFTPH in different tumors.FEBS open bio · 2020Article
- Role of G protein-coupled receptors-microRNA interactions in gastrointestinal pathophysiology.American journal of physiology. Gastrointestinal and liver physiology · 2017Review
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Neurotensin (NT) triggers signaling in human colonic epithelial cells by activating the G protein-coupled receptor, the neurotensin receptor 1 (NTR1). Activated NTR1 traffics from the plasma membrane to early endosomes, and then recycles. Although sustained NT/NTR1 signaling requires efficient NTR1 recycling, little is known about the regulation of NTR1 recycling. We recently showed that NT/NTR1 signaling increases expression of miR-133α. Herein, we studied the mechanism of NT-regulated miR-133α expression and examined the role of miR-133α in intracellular NTR1 trafficking in human NCM460 colonocytes. We found that NT-induced miR-133α upregulation involves the negative transcription regulator, zinc finger E-box binding homeobox 1. Silencing of miR-133α or overexpression of aftiphilin (AFTPH), a binding target of miR-133α, attenuated NTR1 trafficking to plasma membrane in human colonocytes, without affecting NTR1 internalization. We localized AFTPH to early endosomes and the trans-Golgi network (TGN) in unstimulated human colonic epithelial cells. AFTPH overexpression reduced NTR1 localization in early endosomes and increased expression of proteins related to endosomes and the TGN trafficking pathway. AFTPH overexpression and de-acidification of intracellular vesicles increased NTR1 expression. Our results suggest a novel mechanism of GPCR trafficking in human colonic epithelial cells by which a microRNA, miR-133α regulates NTR1 trafficking through its downstream target AFTPH.
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