Evidence map›Paper›PMID 33909502›Full record

ArticleAmerican journal of physiology. Cell physiology2021

Ethanol-induced lymphatic endothelial cell permeability via MAP-kinase regulation.

Matthew Herrera, Patricia Molina, Flavia M Souza-Smith

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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  10. Article
  11. Lymphangiogenesis and Lymphatic Barrier Dysfunction in Renal Fibrosis.International journal of molecular sciences · 2022
    Review
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

3 authors at 1 institution in 1 country.

Matthew HerreraDepartment of Physiology, Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
Patricia MolinaDepartment of Physiology, Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
Flavia M Souza-SmithDepartment of Physiology, Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
Louisiana State University Health Sciences Center New Orleans · US

Funding

Mesenteric Lymphatic / Perilymphatic Adipose Tissue Crosstalk; Mechanism of Alcohol ImmunomodulationK01AA026640 · NIAAA · LSU HEALTH SCIENCES CENTER · PI SOUZA, FLAVIA MOREIRA · 2018 to 2022
$911k
NIAAA NIH HHS K01 AA026640
6 · The paper itself

Abstract

Chronic alcohol alters the immune system enhancing the susceptibility to inflammation, bacterial, and viral infections in alcohol users. We have shown that alcohol causes increased permeability of mesenteric lymphatic vessels in alcohol-fed rats. The mechanisms of alcohol-induced lymphatic leakage are unknown. Endothelial cell monolayer permeability is controlled by junctional proteins complexes called tight junctions (TJ) and adherens junctions (AJ), and each can be regulated by MAPK activation. We hypothesize that ethanol induces lymphatic endothelial cell (LEC) permeability via disruption of LEC TJ through MAPK activation. An in vitro model of rat LECs was used. Ethanol-supplemented medium was added at concentrations of 0, 25, and 50 mM to confluent cells. Resistance-based barrier function, transwell permeability, cell viability, TJ, AJ, and MAPK protein activity, TJ and AJ gene expressions, and the role of p38 MAPK in barrier function regulation were measured. Ethanol increased the permeability of LECs compared to controls that was not associated with decreased cell viability. LECs treated with 50 mM ethanol showed an increase in phosphorylated levels of p38. No significant changes in TJ and AJ gene or protein expressions were observed after ethanol treatment. p38 inhibition prevented ethanol-induced increases in permeability. These findings suggest that p38 may play a role in the regulation of ethanol-induced LEC permeability, but altered permeability may not be associated with decreased TJ or AJ protein expression. Further investigation into junctional protein localization is needed to better understand the effects of ethanol on lymphatic endothelial cell-to-cell contacts and hyperpermeability.

Indexed as

Adherens JunctionsAnimalsAnimals, NewbornAntigens, CDBiological TransportCadherin 5CadherinsCell Membrane PermeabilityClaudin-5DermisDiffusion Chambers, CultureElectric ImpedanceEndothelial CellsEthanolGene Expression RegulationOccludinAntigens, CDCadherin 5CadherinsClaudin-5Cldn5 protein, ratEthanolOccludinOcln protein, ratp38 Mitogen-Activated Protein KinasesTjp1 protein, ratZonula Occludens-1 Proteinalcoholendothelial celllymphaticMAPKtight junction

Identifiers

PMID33909502
PMCPMC8321794
OpenAlexW3158904619

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.