Evidence map›Paper›PMID 33566256›Full record

ArticleInflammation2021

Galectin-1 Inhibited LPS-Induced Autophagy and Apoptosis of Human Periodontal Ligament Stem Cells.

Jiahao Zhang, Xiaohong Dong, Qianqian Yan, Wei Ren, Rui Zhang, Xinyi Jiang, Zhaoli Geng, Xinyi Xu, Chunpeng Liu, Shijie Zhang and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 16 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

12 authors at 4 institutions in 1 country.

Jiahao ZhangDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Xiaohong DongChangle People's Hospital, Weifang, Shandong, 262400, People's Republic of China.
Qianqian YanQufu Stomatological Hospital, Jining, Shandong, 273100, People's Republic of China.
Wei RenDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Rui ZhangDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Xinyi JiangDepartment of Pharmaceutics, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Zhaoli GengDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Xinyi XuDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Chunpeng LiuDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Shijie ZhangDepartment of Orthodontics, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Dongxu LiuDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China. liudongxusdu@163.com.
Yi LiuDepartment of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China. yiliusdu@163.com.ORCID http://orcid.org/0000-0001-9490-1544
Shandong University · CNJinan Stomatological Hospital · CNQilu Hospital of Shandong University · CNWeifang People's Hospital · CN

Funding

Guangdong Basic and Applied Basic Research Foundation NO. 2020A1515010150Key research and development program of Shandong Province NO. 2019GSF108187, 2019GSF108046National Natural Science Foundation of China NO. 81701008Students Research Fund of Shandong University NO.2019298
6 · The paper itself

Abstract

Periodontitis is a widespread human chronic inflammatory disease of the tooth-surrounding tissues, which induces the destruction of periodontium and pathologic loss of teeth among adults. It has been reported that interleukin (IL)-17 was significantly increased in periodontitis patients compared to controls, while galectin-1 (Gal-1) was lower. Interestingly, it is found that Gal-1 treatment reduced systemic IL-17 levels. Hence, the aim of the present study was to explore the effect of Gal-1 on periodontitis development and investigate its underlying mechanism. In this study, Gal-1 was poorly expressed in lipopolysaccharide (LPS)-induced human periodontal ligament stem cells (hPDLSCs), and Gal-1 overexpression attenuated the production of inflammatory cytokines induced by LPS. Moreover, Gal-1 overexpression alleviated LPS-induced cell autophagy and apoptosis and reduced the expressions of IL-17A and IL-17R. Interestingly, IL-17A reversed the effect of Gal-1 on cell autophagy, inflammation, and cell apoptosis induced by the LPS challenge. In conclusion, Gal-1 inhibited LPS-induced autophagy and apoptosis of hPDLSC via regulation of IL-17A expression. Therefore, Gal-1 may have promising potential in regenerating periodontium.

Indexed as

ApoptosisAutophagyCells, CulturedGalectin 1HumansLipopolysaccharidesPeriodontal LigamentStem CellsGalectin 1Lipopolysaccharidesapoptosisautophagygalectin-1 (Gal-1)human periodontal ligament stem cells (hPDLSCs)IL-17A

Identifiers

PMID33566256
OpenAlexW3128074142

What Socratic 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 Socratic graph.