Evidence map›Paper›PMID 34118020›Full record

ArticleMetabolic brain disease2021

Blood-brain barrier leakage and perivascular collagen accumulation precede microvessel rarefaction and memory impairment in a chronic hypertension animal model.

Esra Özkan, Yağmur Çetin-Taş, Emine Şekerdağ, Ali B Kızılırmak, Ali Taş, Erdost Yıldız, Hale Yapıcı-Eser, Serçin Karahüseyinoğlu, Müjdat Zeybel, Yasemin Gürsoy-Özdemir

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In one paragraph

Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Blood-brain barrier leakage years after pre-eclampsia: dynamic contrast-enhanced 7-Tesla MRI study.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2022
    Observational
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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

10 authors at 2 institutions in 2 countries.

Esra ÖzkanKoç University Research Center for Translational Medicine, Istanbul, Turkey. eozkan19@ku.edu.tr.
Yağmur Çetin-TaşKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Emine ŞekerdağKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Ali B KızılırmakKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Ali TaşKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Erdost YıldızKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Hale Yapıcı-EserKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Serçin KarahüseyinoğluKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Müjdat ZeybelKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Yasemin Gürsoy-ÖzdemirKoç University Research Center for Translational Medicine, Istanbul, Turkey.
Koç University · TRNottingham University Hospitals NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension (HT) is one of the main causes of vascular dementia, lead to cognitive decline. Here, we investigated the relationship between cerebral microvessels, pericytes, extracellular matrix (ECM) accumulation, blood-brain barrier (BBB) breakdown, and memory impairment at mid-life in a chronic hypertension animal model. Spontaneously hypertensive rats (SHRs) (n = 20) are chosen for the model and age matched Wistar rats (n = 16) as controls. Changes in brain microvasculature and in vitro experiments are shown with immunofluorescence studies and cognition with open field, novel object recognition, and Y maze tests. There was a significant reduction in pericyte coverage in SHRs (p = 0.021), while the quantitative parameters of the cerebral microvascular network were not different between groups. On the other hand, parenchymal albumin leakage, as a Blood-brain barrier (BBB) breakdown marker, was prominent in SHRs (p = 0.023). Extracellular matrix (ECM) components, collagen type 1, 3 and 4 were significantly increased (accumulated) around microvasculature in SHRs (p = 0.011, p = 0.013, p = 0.037, respectively). Furthermore, in vitro experiments demonstrated that human brain vascular pericytes but not astrocytes and endothelial cells secreted type I collagen upon TGFβ1 exposure pointing out a possible role of pericytes in increased collagen accumulation around cerebral microvasculature due to HT. Furthermore, valsartan treatment decreased the amount of collagen type 1 secreted by pericytes after TGFβ1 exposure. At the time of evaluation, SHRs did not demonstrate cognitive decline and memory impairments. Our results showed that chronic HT causes ECM accumulation and BBB leakage before leading to memory impairments and therefore, pericytes could be a novel target for preventing vascular dementia.

Indexed as

Blood-Brain BarrierHypertensionAnimalsCollagenDisease Models, AnimalEndothelial CellsMicrovesselsRatsRats, WistarCollagenBlood–brain barrierCollagenDementiaPericyteSpontaneously hypertensive ratsValsartan

Identifiers

PMID34118020
OpenAlexW3169540108

What OpenQuestion holds

Textmetadata
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.