Evidence map›Paper›PMID 34299188›Full record

ArticleInternational journal of molecular sciences2021

Molecular Mechanism of Stimulation of Na-K-ATPase by Leukotriene D4 in Intestinal Epithelial Cells.

Niraj Nepal, Subha Arthur, Molly R Butts, Soudamani Singh, Balasubramanian Palaniappan, Uma Sundaram

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. CaFrontiers in pharmacology · 2022
    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

6 authors at 1 institution in 1 country.

Niraj NepalDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.ORCID 0000-0003-1525-3214
Subha ArthurDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.
Molly R ButtsDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.
Soudamani SinghDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.ORCID 0000-0001-6689-9942
Balasubramanian PalaniappanDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.ORCID 0000-0003-2082-7534
Uma SundaramDepartment of Clinical and Translational Sciences, Appalachian Clinical and Translational Science Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.ORCID 0000-0002-9322-6740
Marshall University · US

Funding

NIH HHS DK-108054NIH HHS DK-67420NIH HHS P20GM121299-01U.S. Department of Veterans Affairs BX003443-01
6 · The paper itself

Abstract

Na-K-ATPase provides a favorable transcellular Na gradient required for the functioning of Na-dependent nutrient transporters in intestinal epithelial cells. The primary metabolite for enterocytes is glutamine, which is absorbed via Na-glutamine co-transporter (SN2; SLC38A5) in intestinal crypt cells. SN2 activity is stimulated during chronic intestinal inflammation, at least in part, secondarily to the stimulation of Na-K-ATPase activity. Leukotriene D4 (LTD4) is known to be elevated in the mucosa during chronic enteritis, but the way in which it may regulate Na-K-ATPase is not known. In an in vitro model of rat intestinal epithelial cells (IEC-18), Na-K-ATPase activity was significantly stimulated by LTD4. As LTD4 mediates its action via Ca-dependent protein kinase C (PKC), Ca levels were measured and were found to be increased. Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, also mediated stimulation of Na-K-ATPase like LTD4, while BAPTA-AM (Ca chelator) and calphostin-C (Cal-C; PKC inhibitor) prevented the stimulation of Na-K-ATPase activity. LTD4 caused a significant increase in mRNA and plasma membrane protein expression of Na-K-ATPase α1 and β1 subunits, which was prevented by calphostin-C. These data demonstrate that LTD4 stimulates Na-K-ATPase in intestinal crypt cells secondarily to the transcriptional increase of Na-K-ATPase α1 and β1 subunits, mediated via the Ca-activated PKC pathway.

Indexed as

AnimalsCalciumCells, CulturedCell SurvivalEnteritisEnzyme ActivationEpithelial CellsIntestinesLeukotriene D4Protein Kinase CRatsSodium-Potassium-Exchanging ATPaseCalciumLeukotriene D4Protein Kinase CSodium-Potassium-Exchanging ATPasecrypt cellsintestinal epithelial cellsLTD4Na-K-ATPase

Identifiers

PMID34299188
PMCPMC8303499
OpenAlexW3177500623

What OpenQuestion holds

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Registered trials

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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.