Evidence map›Paper›PMID 34922634›Full record

ArticleHereditas2021

Altered microRNAs in C3H10T1/2 cells induced by p.E95K mutant IHH signaling.

Wei Zhou, Luan Chen, Hao Wu, Ting Wang, Gang Ma, Baocheng Wang, Cong Wang, Na Zhang, Yingtian Zhang, Lin He and 4 more

Open access · goldAbstract read
In one paragraph

Article in Hereditas, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. Review
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

14 authors at 3 institutions in 2 countries.

Wei ZhouDepartment of Obstetrics and Gynecology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangdong, Guangzhou, China.
Luan ChenKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Hao WuKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Ting WangInstitutes of Biomedical Sciences, Fudan University, 200030, Shanghai, China.
Gang MaKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Baocheng WangXinhua Hospital, Shanghai Jiao Tong University School of Medicine, 200093, Shanghai, China.
Cong WangKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Na ZhangKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Yingtian ZhangKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Lin HeKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Shengying QinKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China.
Xiaofang SunDepartment of Obstetrics and Gynecology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangdong, Guangzhou, China. xiaofangsun@gzhmu.edu.cn.
Hai ZhangDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, No. 241, West Huaihai Road, 200030, Shanghai, China. zh1103@shchest.org.
Lu ShenKey Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, 200030, Shanghai, China. yoyomailer@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-0659-2399
Shanghai Jiao Tong University · CNFudan University · CNGuangdong University of Education · CN

Funding

school of medicine, shanghai jiao tong university YG2019QNA51
6 · The paper itself

Abstract

backgroundIndian Hedgehog (IHH), an important cell signaling protein, plays a key regulatory role in development of cartilage and chondrogenesis. Earlier studies have shown that heterozygous missense mutations in IHH gene may cause brachydactyly type A1 (BDA1), an autosomal dominant inheritance disease characterized by apparent shortness or absence of the middle phalanges of all digits. MicroRNAs (miRNAs) have been found to be significant post-transcriptional regulators of gene expression and significantly influence the process of bone-development. Therefore, it is possible that miRNAs are involved in the mechanism underlying the development of BDA1. However, the relationship between miRNAs and the pathogenesis of BDA1 remains unclear.

methodsIn this study, we used microarray-based miRNA profiling to investigate the role of miRNAs in BDA1 by characterization of differentially expressed miRNAs in C3H10T1/2 cell line induced by wild type (WT) and p.E95K mutant (MT) IHH signaling.

resultsOur results identified 6 differentially expressed miRNAs between WT and control (CT) group and 5 differentially expressed miRNAs between MT and CT groups. In particular, miR-135a-1-3p was found to be a significantly differentially expressed miRNA between WT and CT group. Results of dual-luciferase reporter gene experiment successfully discovered Hoxd10 was one of the target gene of miR-135a-1-3p. Additionally, our pathway analysis revealed that the targets of these miRNAs of interest were highly involved with Runx1/2, Notch and collagen-related pathways.

conclusionsTaken together, our findings provided important clue for future study of the process of miRNA-regulation in IHH signaling and novel insights into the regulatory role of miRNA in pathogenesis of BDA1.

Indexed as

BrachydactylyHedgehog ProteinsMicroRNAsAnimalsCell LineGene Expression ProfilingHeterozygoteMiceSignal TransductionHedgehog ProteinsMicroRNAsBrachydactyly type A1Indian hedgehogmicroRNAPathogenesis

Identifiers

PMID34922634
PMCPMC8684136
OpenAlexW4200004123

What OpenQuestion holds

Textmetadata
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.