Evidence map›Paper›PMID 9593763›Full record

ArticleThe Journal of clinical investigation1998

Na-K-2Cl cotransporter gene expression and function during enterocyte differentiation. Modulation of Cl- secretory capacity by butyrate.

J B Matthews, I Hassan, S Meng, S Y Archer, B J Hrnjez, R A Hodin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Intestinal secretory mechanisms and diarrhea.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Review
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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

6 authors at 2 institutions in 1 country.

J B MatthewsDivision of General Surgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. jmatthew@bidmc.harvard.edu
I Hassan
S Meng
S Y Archer
B J Hrnjez
R A Hodin
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

MOLECULAR MECHANISMS OF INTESTINAL ATROPHY/HYPERPLASIAR01DK047186 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HODIN, RICHARD A. · 2000 to 2011
$3.4M
SALT TRANSPORT IN SURGICAL DIARRHEAL DISEASER01DK048010 · NIDDK · UNIVERSITY OF CINCINNATI · PI MATTHEWS, JEFFREY B. · 1999 to 2008
$3.2M
INTESTINAL SECRETION &INFLAMMATION - IMPACT OF AMMONIAR01DK051630 · NIDDK · UNIVERSITY OF CINCINNATI · PI MATTHEWS, JEFFREY B. · 1996 to 2004
$1.6M
MOLECULAR MECHANISMS OF INTESTINAL ATROPHY/HYPERPLASIAR29DK047186 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HODIN, RICHARD A. · 1994 to 1998
–
SALT TRANSPORT IN SURGICAL DIARRHEAL DISEASER29DK048010 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MATTHEWS, JEFFREY B. · 1994 to 1998
–
NIDDK NIH HHS DK-47186NIDDK NIH HHS DK-48010NIDDK NIH HHS DK-51630
6 · The paper itself

Abstract

The basolateral Na-K-2Cl cotransporter (NKCC1) is a key component of the intestinal crypt cell secretory apparatus. Its fate during the transition to absorptive enterocyte and the potential impact of its altered expression on secretory output have not been addressed. In this report, NKCC1 mRNA was found to be expressed in rat jejunal crypt but not villus cells. Butyrate treatment of intestinal epithelial HT29 cells induced a differentiation pattern that recapitulated the rat intestinal crypt-villus axis, with NKCC1 mRNA levels decreasing in a time- and dose-dependent fashion in parallel with upregulation of apical brush-border markers. Butyrate but not acetate or proprionate decreased basal and cAMP-stimulated bumetanide-sensitive K+ (86Rb) uptake in both HT29 cells and the Cl--secreting T84 line. Butyrate markedly decreased transepithelial Cl- secretion in confluent T84 monolayers without effect on cAMP-regulated apical Cl- efflux. We conclude that NKCC1 regulation during enterocyte differentiation occurs at the level of gene expression, and that selective downregulation of NKCC1 gene expression and function by butyrate leads to a profound decrease in transepithelial Cl- secretion. These data emphasize the importance of NKCC1 in determining epithelial secretory capacity and suggest the possibility of modulation of the enterocytic transport phenotype as therapy for diarrheal disorders.

Indexed as

AnimalsBumetanideButyratesButyric AcidCarrier ProteinsCell DifferentiationCell LineChloridesColforsinCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorDiarrheaDown-RegulationGene Expression Regulation, DevelopmentalHumansIntestinesBumetanideButyratesButyric AcidCarrier ProteinsCFTR protein, humanChloridesColforsinCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorPotassiumProtein Synthesis InhibitorsRNA, MessengerSodium-Potassium-Chloride Symporters

Identifiers

PMID9593763
PMCPMC508795
OpenAlexW2078844281

What OpenQuestion holds

Textmetadata
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.