Evidence map›Paper›PMID 26168035›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

17β-Estradiol Ameliorates Tight Junction Disruption via Repression of MMP Transcription.

Wonho Na, Jee Youn Lee, Won-Sun Kim, Tae Young Yune, Bong-Gun Ju

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  5. Understanding the Blood-Brain Barrier: From Physiology to Pathology.Advances in experimental medicine and biology · 2025
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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

5 authors at 2 institutions in 1 country.

Wonho NaDepartment of Life Science (W.N., W.-S.K., B.-G.J.), Sogang University, Seoul 121-742, Korea; and Age-Related and Brain Diseases Research Center (J.Y.L., T.Y.Y.) and Department of Biochemistry and Molecular Biology (T.Y.Y.), School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
Jee Youn LeeDepartment of Life Science (W.N., W.-S.K., B.-G.J.), Sogang University, Seoul 121-742, Korea; and Age-Related and Brain Diseases Research Center (J.Y.L., T.Y.Y.) and Department of Biochemistry and Molecular Biology (T.Y.Y.), School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
Won-Sun KimDepartment of Life Science (W.N., W.-S.K., B.-G.J.), Sogang University, Seoul 121-742, Korea; and Age-Related and Brain Diseases Research Center (J.Y.L., T.Y.Y.) and Department of Biochemistry and Molecular Biology (T.Y.Y.), School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
Tae Young YuneDepartment of Life Science (W.N., W.-S.K., B.-G.J.), Sogang University, Seoul 121-742, Korea; and Age-Related and Brain Diseases Research Center (J.Y.L., T.Y.Y.) and Department of Biochemistry and Molecular Biology (T.Y.Y.), School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
Bong-Gun JuDepartment of Life Science (W.N., W.-S.K., B.-G.J.), Sogang University, Seoul 121-742, Korea; and Age-Related and Brain Diseases Research Center (J.Y.L., T.Y.Y.) and Department of Biochemistry and Molecular Biology (T.Y.Y.), School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
Sogang University · KRKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-brain barrier (BBB) or blood-spinal cord barrier (BSCB) formed by capillary endothelial cells provides a physical wall between the central nervous system (CNS) and circulating blood with highly selective permeability. BBB/BSCB disruption by activation of matrix metalloproteinases (MMPs) has been shown to result in further neurological damage after CNS injury. Recently it has been discovered that estrogen attenuates BBB/BSCB disruption in in vitro and in vivo models. However, the molecular mechanism underlying the estrogen-mediated attenuation of BBB/BSCB disruption has not been elucidated fully. In the present study, we found that 17β-estradiol (E2) suppresses nuclear factor-κB-dependent MMP-1b, MMP-2, MMP-3, MMP-9, MMP-10, and MMP-13 gene activation in microvessel endothelial bEnd.3 cells subjected to oxygen and glucose deprivation/reperfusion injury. E2 induced the recruitment of ERα and nuclear receptor corepressor to the nuclear factor-κB binding site on the MMPs' gene promoters. Consistently, ER antagonist ICI 182.780 showed opposite effects of E2. We further found that E2 attenuates tight junction disruption through the decreased degradation of tight junction proteins in bEnd.3 cells subjected to oxygen and glucose deprivation-reperfusion injury. In addition, E2 suppressed the up-regulation of MMP expression, leading to a decreased BSCB disruption in the injured spinal cord. In conclusion, we discovered the molecular mechanism underlying the protective role of estrogenin BBB/BSCB disruption using an in vitro and in vivo model. Our study suggests that estrogens may provide a potential therapeutic intervention for preserving BBB/BSCB integrity after CNS injury.

Indexed as

AnimalsBlood-Brain BarrierBrain InjuriesCell LineElectric ImpedanceEndothelial CellsEnzyme ActivationEstradiolEstrogen Receptor alphaEstrogen Receptor AntagonistsFulvestrantMaleMatrix MetalloproteinasesMiceNF-kappa BPromoter Regions, GeneticEstradiolEstrogen Receptor alphaEstrogen Receptor AntagonistsFulvestrantMatrix MetalloproteinasesNF-kappa BRNA, Small Interfering

Identifiers

PMID26168035
PMCPMC5414681
OpenAlexW2205239210

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.