Evidence map›Paper›PMID 31928157›Full record

ArticleJournal of the American Heart Association2020

Endothelial Immune Activation by Medin: Potential Role in Cerebrovascular Disease and Reversal by Monosialoganglioside-Containing Nanoliposomes.

Nina Karamanova, Seth Truran, Geidy E Serrano, Thomas G Beach, Jillian Madine, Volkmar Weissig, Hannah A Davies, Jaimeson Veldhuizen, Mehdi Nikkhah, Michael Hansen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  6. Exercise to Mitigate Cerebrovascular Aging: A Geroscience Perspective.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Review
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  11. Review
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  14. Review
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  16. Article
  17. Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
  19. Article
  20. 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

14 authors at 5 institutions in 2 countries.

Nina KaramanovaPhoenix Veterans Affairs Phoenix AZ.
Seth TruranPhoenix Veterans Affairs Phoenix AZ.
Geidy E SerranoBanner Sun Health Research Institute Sun City AZ.
Thomas G BeachBanner Sun Health Research Institute Sun City AZ.
Jillian MadineUniversity of Liverpool United Kingdom.
Volkmar WeissigMidwestern University Glendale AZ.
Hannah A DaviesUniversity of Liverpool United Kingdom.
Jaimeson VeldhuizenArizona State University Tempe AZ.
Mehdi NikkhahPhoenix Veterans Affairs Phoenix AZ.
Michael HansenPhoenix Veterans Affairs Phoenix AZ.
Weiyang ZhangPhoenix Veterans Affairs Phoenix AZ.
Karen D'SouzaPhoenix Veterans Affairs Phoenix AZ.
Daniel A FrancoPhoenix Veterans Affairs Phoenix AZ.
Raymond Q MigrinoPhoenix Veterans Affairs Phoenix AZ.
Phoenix VA Health Care System · USBanner Sun Health Research Institute · USUniversity of Liverpool · GBArizona State University · USMidwestern University · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
APP/AB/Tau biochemistry in transgenic mice, familial and sporadic ADR01AG019795 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI ROHER, ALEX E · 2001 to 2013
$3.8M
Discovering novel mechanisms for aging-related dementia: probing medin and abeta vasculopathyI01BX003767 · VA · PHOENIX VA HEALTH CARE SYSTEM · PI MIGRINO, RAYMOND QUEZON · 2017 to 2024
–
BLRD VA I01 BX003767British Heart Foundation FS/12/61/29877NIA NIH HHS P30 AG019610NIA NIH HHS R01 AG019795NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

Background The function of medin, one of the most common human amyloid proteins that accumulates in the vasculature with aging, remains unknown. We aim to probe medin's role in cerebrovascular disease by comparing cerebral arterial medin content between cognitively normal and vascular dementia (VaD) patients and studying its effects on endothelial cell (EC) immune activation and neuroinflammation. We also tested whether monosialoganglioside-containing nanoliposomes could reverse medin's adverse effects. Methods and Results Cerebral artery medin and astrocyte activation were measured and compared between VaD and cognitively normal elderly brain donors. ECs were exposed to physiologic dose of medin (5 μmol/L), and viability and immune activation (interleukin-8, interleukin-6, intercellular adhesion molecule-1, and plasminogen activator inhibitor-1) were measured without or with monosialoganglioside-containing nanoliposomes (300 μg/mL). Astrocytes were exposed to vehicle, medin, medin-treated ECs, or their conditioned media, and interleukin-8 production was compared. Cerebral collateral arterial and parenchymal arteriole medin, white matter lesion scores, and astrocyte activation were higher in VaD versus cognitively normal donors. Medin induced EC immune activation (increased interleukin-8, interleukin-6, intercellular adhesion molecule-1, and plasminogen activator inhibitor-1) and reduced EC viability, which were reversed by monosialoganglioside-containing nanoliposomes. Interleukin-8 production was augmented when astrocytes were exposed to medin-treated ECs or their conditioned media. Conclusions Cerebral arterial medin is higher in VaD compared with cognitively normal patients. Medin induces EC immune activation that modulates astrocyte activation, and its effects are reversed by monosialoganglioside-containing nanoliposomes. Medin is a candidate novel risk factor for aging-related cerebrovascular disease and VaD.

Indexed as

NanoparticlesAgedAged, 80 and overAntigens, SurfaceAstrocytesCase-Control StudiesCell CommunicationCells, CulturedCell SurvivalCerebral ArteriesCoculture TechniquesDementia, VascularEndothelial CellsFemaleGangliosidesHumansAntigens, SurfaceGangliosidesLiposomesMFGE8 protein, humanMilk Proteinssialogangliosidesagingamyloidcerebrovascular diseaseinflammationvascular dementia

Identifiers

PMID31928157
PMCPMC7033828
OpenAlexW3000646041

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.