Evidence map›Paper›PMID 30759717›Full record

ArticleInternational journal of molecular sciences2019

MIST1, an Inductive Signal for Salivary Amylase in Mesenchymal Stem Cells.

Mahmoud Mona, Rehae Miller, Hui Li, Yun-Jong Park, Raafi Zaman, Li-Jun Yang, Seunghee Cha

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Mahmoud MonaOral and Maxillofacial Diagnostic Sciences, University of Florida College of Dentistry, Gainesville, FL 32610, USA. mmona@dental.ufl.edu.ORCID 0000-0002-2626-8318
Rehae MillerOral and Maxillofacial Diagnostic Sciences, University of Florida College of Dentistry, Gainesville, FL 32610, USA. RMiller2@dental.ufl.edu.
Hui LiPathology, University of Florida College of Medicine, Gainesville, FL 32610, USA. lih@ufl.edu.
Yun-Jong ParkPharmacology, University of North Carolina College of Medicine, Chapel Hill, NC 27599, USA. yjpark7604@gmail.com.
Raafi ZamanOral and Maxillofacial Diagnostic Sciences, University of Florida College of Dentistry, Gainesville, FL 32610, USA. raafiz@ufl.edu.
Li-Jun YangPathology, University of Florida College of Medicine, Gainesville, FL 32610, USA. yanglj@pathology.ufl.edu.
Seunghee ChaOral and Maxillofacial Diagnostic Sciences, University of Florida College of Dentistry, Gainesville, FL 32610, USA. scha@dental.ufl.edu.
University of Florida · USUniversity of North Carolina at Chapel Hill · US

Funding

Comprehensive Training Program in Oral BiologyT90DE021990 · NIDCR · UNIVERSITY OF FLORIDA · PI Jose A Lemos · 2011 to 2026
$8.2M
NIDCR NIH HHS DE021990NIDCR NIH HHS DE02726NIDCR NIH HHS T90 DE021990
6 · The paper itself

Abstract

Sjögren's syndrome (SjS) is an autoimmune disease that destroys the salivary glands and results in severe dry mouth. Mesenchymal stem cell (MSC) transplantation has been recently proposed as a promising therapy for restoring cells in multiple degenerative diseases. We have recently utilized advanced proteomics biochemical assays to identify the key molecules involved in the mesenchymal-epithelial transition (MET) of co-cultured mouse bone-marrow-derived MSCs mMSCs with primary salivary gland cells. Among the multiple transcription factors (TFs) that were differentially expressed, two major TFs were selected: muscle, intestine, and stomach expression-1 (MIST1) and transcription factor E2a (TCF3). These factors were assessed in the current study for their ability to drive the expression of acinar cell marker, alpha-salivary amylase 1 (AMY1), and ductal cell marker, cytokeratin19 (CK19), in vitro. Overexpression of MIST1-induced AMY1 expression while it had little effect on CK19 expression. In contrast, TCF3 induced neither of those cellular markers. Furthermore, we have identified that mMSCs express muscarinic-type 3 receptor (M3R) mainly in the cytoplasm and aquaporin 5 (AQP5) in the nucleus. While MIST1 did not alter M3R levels in mMSCs, a TCF3 overexpression downregulated M3R expressions in mMSCs. The mechanisms for such differential regulation of glandular markers by these TFs warrant further investigation.

Indexed as

AmylasesAnimalsAquaporin 5Basic Helix-Loop-Helix ProteinsBiomarkersCells, CulturedCoculture TechniquesDown-RegulationGene Expression RegulationHumansKeratin-19Mesenchymal Stem CellsMiceMice, Inbred C57BLProteomicsSalivary GlandsAmylasesAquaporin 5Basic Helix-Loop-Helix ProteinsBHLHA15 protein, humanBiomarkersKeratin-19Transcription Factorsalpha-salivary amylase 1MIST1mouse bone-marrow-mesenchymal stem cellssalivary precursorsSjögren’s syndromeTCF3

Identifiers

PMID30759717
PMCPMC6387180
OpenAlexW2912531697

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.