Evidence map›Paper›PMID 33607992›Full record

ArticleRespiratory research2021

PGC-1α regulates airway epithelial barrier dysfunction induced by house dust mite.

Tsutomu Saito, Tomohiro Ichikawa, Tadahisa Numakura, Mitsuhiro Yamada, Akira Koarai, Naoya Fujino, Koji Murakami, Shun Yamanaka, Yusaku Sasaki, Yorihiko Kyogoku and 7 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Role and regulators of NFrontiers in pharmacology · 2024
    Review
  5. Upregulation of PGC-1α expression by pioglitazone mediates prevention of sepsis-induced acute lung injury.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  6. Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 1 country.

Tsutomu SaitoDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Tomohiro IchikawaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan. ichikawa@rm.med.tohoku.ac.jp.ORCID http://orcid.org/0000-0003-0093-6362
Tadahisa NumakuraDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Mitsuhiro YamadaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Akira KoaraiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Naoya FujinoDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Koji MurakamiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Shun YamanakaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Yusaku SasakiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Yorihiko KyogokuDepartment of Respiratory Medicine, Sendai City Hospital, Sendai, Japan.
Koji ItakuraDepartment of Respiratory Medicine, Osaki Citizen Hospital, Osaki, Miyagi, Japan.
Hirohito SanoDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Katsuya TakitaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Rie TanakaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Tsutomu TamadaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Masakazu IchinoseDepartment of Respiratory Medicine, Osaki Citizen Hospital, Osaki, Miyagi, Japan.
Hisatoshi SugiuraDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Tohoku University · JPOsaki Citizen Hospital · JPSendai City Hospital · JP

Funding

he Practical Research Project for Allergic Diseases and Immunology from Japan Agency for Medical Research and Development, AMED #16ek0410018h0002The Japan Society for the Promotion of Science #18K08166the Practical Research Project for Allergic Diseases and Immunology from Japan Agency for Medical Research and Development, AMED #16ek040036h0001the Practical Research Project for Allergic Diseases and Immunology from Japan Agency for Medical Research and Development, AMED #17ek0410036h0002
6 · The paper itself

Abstract

backgroundThe airway epithelial barrier function is disrupted in the airways of asthmatic patients. Abnormal mitochondrial biogenesis is reportedly involved in the pathogenesis of asthma. However, the role of mitochondrial biogenesis in the airway barrier dysfunction has not been elucidated yet. This study aimed to clarify whether the peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α), a central regulator of mitochondrial biogenesis, is involved in the disruption of the airway barrier function induced by aeroallergens.

methodsBEAS-2B cells were exposed to house dust mite (HDM) and the expressions of PGC-1α and E-cadherin, a junctional protein, were examined by immunoblotting. The effect of SRT1720, a PGC-1α activator, was investigated by immunoblotting, immunocytochemistry, and measuring the transepithelial electrical resistance (TEER) on the HDM-induced reduction in mitochondrial biogenesis markers and junctional proteins in airway bronchial epithelial cells. Furthermore,the effects of protease activated receptor 2 (PAR2) inhibitor, GB83, Toll-like receptor 4 (TLR4) inhibitor, lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), protease inhibitors including E64 and 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) on the HDM-induced barrier dysfunction were investigated.

resultsThe amounts of PGC-1α and E-cadherin in the HDM-treated cells were significantly decreased compared to the vehicle-treated cells. SRT1720 restored the expressions of PGC-1α and E-cadherin reduced by HDM in BEAS-2B cells. Treatment with SRT1720 also significantly ameliorated the HDM-induced reduction in TEER. In addition, GB83, LPS-RS, E64 and AEBSF prevented the HDM-induced reduction in the expression of PGC1α and E-cadherin.

conclusionsThe current study demonstrated that HDM disrupted the airway barrier function through the PAR2/TLR4/PGC-1α-dependent pathway. The modulation of this pathway could be a new approach for the treatment of asthma.

Indexed as

PyroglyphidaeAnimalsAsthmaBronchiCell LineCells, CulturedDisease Models, AnimalElectric ImpedanceEpithelial CellsFemaleHumansMiceMice, Inbred C57BLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRespiratory MucosaSignal TransductionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAirway barrier dysfunctionAsthmaHouse dust mitePGC-1α

Identifiers

PMID33607992
PMCPMC7893966
OpenAlexW3118612842

What OpenQuestion holds

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LicenceCC BY
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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.