Evidence map›Paper›PMID 31887550›Full record

ArticleMolecular therapy. Nucleic acids2020

H19 Increases IL-17A/IL-23 Releases via Regulating VDR by Interacting with miR675-5p/miR22-5p in Ankylosing Spondylitis.

Xu Zhang, Shuang Ji, Guoqi Cai, Zhipeng Pan, Renfang Han, Yaping Yuan, Shanshan Xu, Jiajia Yang, Xingxing Hu, Mengya Chen and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 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

19 authors at 3 institutions in 2 countries.

Xu ZhangDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Shuang JiDepartment of Respiratory and Critical Care Medicine, First Affiliated Hospital of Anhui Medical University, Hefei, China.
Guoqi CaiDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Zhipeng PanDepartment of Medical Oncology, First Affiliated Hospital of Anhui Medical University, Hefei, China.
Renfang HanDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Yaping YuanDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Shanshan XuDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Jiajia YangDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Xingxing HuDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Mengya ChenDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Meng WuDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Yubo MaDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Jixiang DengDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Xing GaoDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Shiyang GuanDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China.
Shengqian XuDepartment of Rheumatism and Immunity, First Affiliated Hospital of Anhui Medical University, Hefei, China.
Zongwen ShuaiDepartment of Rheumatism and Immunity, First Affiliated Hospital of Anhui Medical University, Hefei, China.
Laura LaslettMenzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
Faming PanDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China; Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, China. Electronic address: famingpan@ahmu.edu.cn.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CNUniversity of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) H19 is associated with inflammatory diseases, but the molecular mechanism of H19 in the inflammatory process of ankylosing spondylitis (AS) is unclear. Here, we investigated the role of H19 and its downstream molecules in the inflammation of AS by microarray analysis, qRT-PCR, western blot, and dual-luciferase reporter assay. H19 small interfering RNA (siRNA) (Si-H19) and adenovirus (AD-H19) were used to decrease and increase H19 expression, respectively. 42 annotated lncRNAs were identified, and H19 was overexpressed. H19, vitamin D receptor (VDR), and transforming growth factor β (TGF-β) can bind to microRNA22-5p (miR22-5p) and miR675-5p. Si-H19 significantly downregulated miR22-5p and upregulated miR675-5p expression; Si-H19 decreased the protein and mRNA expression of VDR and decreased the cytokine and mRNA levels of interleukin-17A (IL-17A) and IL-23. These results were verified by AD-H19. In addition, miR22-5p and miR675-5p inhibitors increased the protein and mRNA expression of VDR and increased the cytokine and mRNA levels of IL-17A and IL-23. These results were also confirmed by miRNA mimics. Furthermore, H19 directly interfered with miR22-5p and miR675-5p expression, whereas the two miRNAs directly inhibited VDR expression. Overall, the H19-miR22-5p/miR675-5p-VDR-IL-17A/IL-23 signaling pathways have important roles in the pathogenesis of AS.

Indexed as

ankylosing spondylitiscytokinesH19IL-17AIL-23miR22miR675non-coding RNAVDR

Identifiers

PMID31887550
PMCPMC6938967
OpenAlexW2991334742

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.