Evidence map›Paper›PMID 27881852›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2017

Macrophage-derived exosomes induce inflammatory factors in endothelial cells under hypertensive conditions.

Mayuko Osada-Oka, Masayuki Shiota, Yasukatsu Izumi, Masaki Nishiyama, Masako Tanaka, Takehiro Yamaguchi, Emi Sakurai, Katsuyuki Miura, Hiroshi Iwao

Abstract read
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In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 125 citations in OpenAlex.

  1. The theory of the inflammatory ecosystem.Science China. Life sciences · 2026
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  9. Extracellular vesicles in preeclampsia: drivers of vascular dysfunction and inflammation.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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17 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Mayuko Osada-OkaFood Hygiene and Environmental Health Division of Applied Life Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto, Japan.
Masayuki ShiotaDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Yasukatsu IzumiDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Masaki NishiyamaDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Masako TanakaApplied Pharmacology and Therapeutics, Osaka City University Medical School, Osaka, Japan.
Takehiro YamaguchiDepartment of Bacteriology, Niigata University Graduate School of Medicine, Niigata, Japan.
Emi SakuraiDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Katsuyuki MiuraDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Hiroshi IwaoDepartment of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Osaka City University · JPNiigata University · JPShitennoji University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is one of the most important cardiovascular risk factors and results in macrophage infiltration of blood vessels. However, how macrophages coordinate inflammatory responses with endothelial cells (ECs) remains unclear. In this study, we investigated whether exosomes upregulate the expression of inflammatory factors in ECs under hypertensive conditions. Hypertension was induced in rats by continuous infusion of angiotensin II (Ang II). Exosomes were purified from rat serum by density gradient and ultracentrifugation and used to stimulate human coronary artery ECs (HCAECs). Moreover, the interactions between HCAECs and exosomes from human THP-1-derived macrophages were analyzed. Administration of Ang II enhanced the expression of CD68, a macrophage marker, in rat hearts, suggesting enhanced infiltration of macrophages. In addition, the expression of intracellular adhesion molecule-1 (ICAM1) and plasminogen activator inhibitor-1 (PAI-1), a proinflammatory factor, was increased in hypertensive rat hearts compared with control rats. CD68 protein expression and an increase in the expression of some exosome markers were detected in exosomes from hypertensive rat serum. Moreover, the exosomes upregulated the expression levels of ICAM1 and PAI-1 in HCAECs. The level of miR-17, a negative regulator of ICAM1 expression, was markedly decreased in exosomes from hypertensive rat serum compared with exosomes from control rats. Interestingly, Ang II-stimulated THP-1-derived exosomes also enhanced the expression of ICAM1 and PAI-1 and contained reduced levels of miR-17 compared with exosomes from unstimulated cells. These results suggest that inflammation of ECs under hypertensive conditions is caused, at least in part, by macrophage-derived exosomes.

Indexed as

Angiotensin IIAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeEndothelial CellsExosomesHypertensionInflammationIntercellular Adhesion Molecule-1MacrophagesMalePlasminogen Activator Inhibitor 1RatsRats, WistarAngiotensin IIAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 antigen, humanCD68 MoleculeIntercellular Adhesion Molecule-1Plasminogen Activator Inhibitor 1

Identifiers

PMID27881852
OpenAlexW2556974751

What OpenQuestion holds

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Read underepoch 390

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.