Evidence map›Paper›PMID 29285169›Full record

ArticleExperimental and therapeutic medicine2017

miR-30b regulates chondrogenic differentiation of mouse embryo-derived stem cells by targeting SOX9.

Qingde Wa, Peiheng He, Shuai Huang, Jianwei Zuo, Xing Li, Jinsong Zhu, Song Hong, Guoqing Lv, Dongfeng Cai, Dongliang Xu and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. 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
0.7field-weighted citation impact, top 27% 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, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. MiR-30 Family: A Novel Avenue for Treating Bone and Joint Diseases?International journal of medical sciences · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
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.

Qingde WaDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Peiheng HeDepartment of Orthopedic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Shuai HuangDepartment of Orthopedic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Jianwei ZuoDepartment of Sports Medicine, Shenzhen Hospital of Peking University, Shenzhen, Guangdong 518036, P.R. China.
Xing LiDepartment of Orthopedic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Jinsong ZhuDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Song HongDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Guoqing LvDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Dongfeng CaiDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Dongliang XuDepartment of Orthopedic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Xuenong ZouDepartment of Orthopedic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Yi LiuDepartment of Orthopedic Surgery, The First Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Affiliated Hospital of Zunyi Medical College · CNSun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNPeking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the mechanisms underlying microRNA (miRNA)-mediated regulation of chondrogenic differentiation. Mouse embryo-derived stem cells C3H10T1/2 were cultured and chondrogenic differentiation was induced using transforming growth factor-β3 (TGF-β3). In addition, miRNA expression profiles were detected via miRNA array analysis, and quantitative polymerase chain reaction was performed to verify the differentially expressed miRNAs. Furthermore, bioinformatics software was used to predict the putative targets and the prediction was validated by dual-luciferase reporter assays and western blot analysis. In addition, cell proliferation and glycosaminoglycans were measured by a direct cell count method and alcian blue staining, respectively. Compared with the control group, 86 miRNAs were identified as differentially expressed in TGF-β3-induced cells and the expression levels of 28 miRNAs were increased while the remaining 58 miRNAs exhibited a decline in expression. Amongst the differentially expressed miRNAs, miR-30b expression was observed to have significantly decreased during chondrogenic differentiation. SOX9 is a target gene of miR-30b, and miR-30b inhibits SOX9 expression during chondrogenic differentiation. Furthermore, the alcian blue staining results demonstrated that miR-30b inhibited early chondrogenic differentiation. However, the data of the present study indicated that miR-30b had no influence on C3H10T1/2 cell line proliferation. In conclusion, miR-30b is a key negative regulator of TGF-β3-induced C3H10T1/2 cell chondrogenic differentiation, which functions by directly targeting SOX9.

Indexed as

chondrogenic differentiationmiR-30bmouse embryo-derived stem cellsSOX9target

Identifiers

PMID29285169
PMCPMC5740517
OpenAlexW2766444541

What OpenQuestion 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 OpenQuestion graph.