Evidence map›Paper›PMID 31964467›Full record

ArticleBMB reports2020

PEP-1-GLRX1 protein exhibits anti-inflammatory effects by inhibiting the activation of MAPK and NF-κB pathways in Raw 264.7 cells.

Min Jea Shin, Dae Won Kim, Yeon Joo Choi, Hyun Ju Cha, Sung Ho Lee, Jinseu Park, Kyu Hyung Han, Won Sik Eum, Soo Young Choi

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Min Jea ShinDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Dae Won KimDepartment of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, Korea.
Yeon Joo ChoiDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Hyun Ju ChaDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Sung Ho LeeDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252; Genesen Inc., Seoul 06181, Korea.
Jinseu ParkDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Kyu Hyung HanDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Won Sik EumDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Soo Young ChoiDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Hallym University · KRGangneung–Wonju National University · KRSangmyung University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases. [BMB Reports 2020; 53(2): 106-111].

Indexed as

PeptidesAnimalsAnti-Inflammatory AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsCysteamineEdemaGlutaredoxinsInflammationLipopolysaccharidesMaleMiceMice, Inbred ICRMitogen-Activated Protein KinasesNF-kappa BNitric Oxide Synthase Type IIAnti-Inflammatory AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsCysteamineGlutaredoxinsLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BNitric Oxide Synthase Type IIPep-1 peptidePeptidesTetradecanoylphorbol Acetate

Identifiers

PMID31964467
PMCPMC7061214
OpenAlexW3009087776

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.