Evidence map›Paper›PMID 33000443›Full record

ReviewCardiovascular engineering and technology2021

Endothelial Glycocalyx-Mediated Intercellular Interactions: Mechanisms and Implications for Atherosclerosis and Cancer Metastasis.

Solomon A Mensah, Alina A Nersesyan, Eno E Ebong

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular engineering and technology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  4. The Glycocalyx: The Importance of Sugar Coating the Blood-Brain Barrier.International journal of molecular sciences · 2024
    Review
  5. Article
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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

3 authors at 2 institutions in 1 country.

Solomon A MensahDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Alina A NersesyanDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Eno E EbongDepartment of Bioengineering, Northeastern University, Boston, MA, USA. e.ebong@northeastern.edu.ORCID 0000-0001-9483-1443
Northeastern University · USWorcester Polytechnic Institute · US

Funding

Atheroprotective vs. Atherogenic Glycocalyx Mechanotransduction MechanismsK01HL125499 · NHLBI · NORTHEASTERN UNIVERSITY · PI EBONG, ENO ESSIEN · 2015 to 2019
$770k
NHLBI NIH HHS K01 HL125499
6 · The paper itself

Abstract

purposeThe endothelial glycocalyx (GCX) plays a critical role in the health of the vascular system. Degradation of the GCX has been implicated in the onset of diseases like atherosclerosis and cancer because it disrupts endothelial cell (EC) function that is meant to protect from atherosclerosis and cancer. Examples of such EC function include interendothelial cell communication via gap junctions and receptor-mediated interactions between endothelial and tumor cells. This review focuses on GCX-dependent regulation of these intercellular interactions in healthy and diseased states. The ultimate goal is to build new knowledge that can be applied to developing GCX regeneration strategies that can control intercellular interaction in order to combat the progression of diseases such as atherosclerosis and cancer.

methodsIn vitro and in vivo studies were conducted to determine the baseline expression of GCX in physiologically relevant conditions. Chemical and mechanical GCX degradation approaches were employed to degrade the GCX. The impact of intact versus degraded GCX on intercellular interactions was assessed using cytochemistry, histochemistry, a Lucifer yellow dye transfer assay, and confocal, intravital, and scanning electron microscopy techniques.

resultsRelevant to atherosclerosis, we found that GCX stability determines the expression and functionality of Cx43 in gap junction-mediated EC-to-EC communication. Relevant to cancer metastasis, we found that destabilizing the GCX through either disturbed flow-induced or enzyme induced GCX degradation results in increased E-selectin receptor-mediated EC-tumor cell interactions.

conclusionOur findings lay a foundation for future endothelial GCX-targeted therapy, to control intercellular interactions and limit the progression of atherosclerosis and cancer.

Indexed as

AtherosclerosisNeoplasmsCell CommunicationEndothelial CellsGap JunctionsGlycocalyxHumansAtherosclerosisCancer metastasisEndothelial cellsGlycocalyxHeparan sulfateSialic acid

Identifiers

PMID33000443
PMCPMC7904750
OpenAlexW3089770365

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.