Evidence map›Paper›PMID 37762395›Full record

ArticleInternational journal of molecular sciences2023

Gintonin-Induced Wound-Healing-Related Responses Involve Epidermal-Growth-Factor-like Effects in Keratinocytes.

Kyung-Jong Won, Rami Lee, Sun-Hye Choi, Ji-Hun Kim, Sung-Hee Hwang, Seung-Yeol Nah

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 9 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

6 authors at 3 institutions in 1 country.

Kyung-Jong WonDepartment of Physiology and Medical Science, College of Medicine, Konkuk University, Chungju 27478, Republic of Korea.ORCID 0000-0001-7677-4641
Rami LeeGinsentology Research Laboratory, Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Republic of Korea.ORCID 0000-0002-0179-7563
Sun-Hye ChoiDepartment of Animal Health, College of Health and Medical Services, Osan University, Osan 18119, Republic of Korea.
Ji-Hun KimGinsentology Research Laboratory, Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Republic of Korea.
Sung-Hee HwangDepartment of Pharmaceutical Engineering, College of Health Sciences, Sangji University, Wonju 26339, Republic of Korea.
Seung-Yeol NahGinsentology Research Laboratory, Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Republic of Korea.ORCID 0000-0001-9697-4763
Konkuk University · KROsan University · KRSangji University · KR

Funding

National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) 2023R1A2C1003481National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) NRF-2020R1A2C1101901National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) NRF-2020R1F1A1067427
6 · The paper itself

Abstract

Epidermal growth factor (EGF) receptor activation and related downstream signaling pathways are known to be one of the major mechanisms of the proliferation and migration of keratinocytes. The heparin-binding EGF-like growth factor (HB-EGF) binds to EGF receptors and stimulates keratinocyte proliferation and migration. Gintonin, a novel ginseng compound, is a lysophosphatidic acid (LPA) receptor ligand. Gintonin has skin-wound-healing effects. However, the underlying mechanisms for these gintonin actions remain unclear. In this study, we aimed to elucidate the involvement of EGFRs in gintonin-induced wound repair in HaCaT keratinocytes. In this study, a water-soluble tetrazolium salt-based assay, a modified Boyden chamber migration assay, and immunoblotting were performed. Gintonin increased EGF receptor activation in HaCaT cells. However, the gintonin-induced phosphorylation of the EGF receptor was markedly reduced via treatment with the LPA inhibitor Ki16425 or the EGF receptor inhibitor erlotinib. Gintonin-enhanced proliferation and migration were blocked by the EGF receptor inhibitors (erlotinib and AG1478). Additionally, gintonin stimulated the expression and release of HB-EGF in HaCaT cells. EGF receptor inhibitors blocked gintonin-enhanced HB-EGF expression. These results indicate that the wound-healing effects of gintonin are closely related to the collaboration between EGF receptor activation and HB-EGF release-mediated downstream signaling pathways.

Indexed as

Epidermal Growth FactorKeratinocytesErbB ReceptorsErlotinib HydrochlorideHeparin-binding EGF-like Growth FactorPlant ExtractsEpidermal Growth FactorErbB ReceptorsErlotinib HydrochloridegintoninHeparin-binding EGF-like Growth FactorPlant Extractsepidermal growth factor receptorgintoninkeratinocyteproliferationskinwound healing

Identifiers

PMID37762395
PMCPMC10531430
OpenAlexW4386785282

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.