Evidence map›Paper›PMID 38982418›Full record

ArticleJournal of orthopaedic surgery and research2024

SP1 regulates BMSC osteogenic differentiation through the miR-133a-3p/MAPK3 axis : SP1 regulates osteogenic differentiation of BMSCs.

Liying Zhong, Yehai Sun, Cong Wang, Runzhi Liu, Wenjuan Ru, Wei Dai, Ting Xiong, Aimin Zhong, Shundong Li

Abstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. LINC00341 promotes fracture healing through downregulation of miR-133a-3p.Journal of orthopaedic surgery and research · 2025
    Article
  4. Article
  5. Circulating miRNAs are associated with successful bone regeneration.Frontiers in bioengineering and biotechnology · 2025
    Article
  6. 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

9 authors.

Liying ZhongDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Yehai SunDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Cong WangDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Runzhi LiuDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Wenjuan RuDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Wei DaiDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Ting XiongDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Aimin ZhongDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China.
Shundong LiDepartment of Geriatrics, The Third Hospital of Changsha, No. 176 Laodongxi Road, Tianxin District, Changsha, Hunan Province, 410015, China. lishundong0818@163.com.

Funding

Natural Science Foundation of Changsha kq2208460
6 · The paper itself

Abstract

backgroundThe progression of osteoporosis (OP) can dramatically increase the risk of fractures, which seriously disturb the life of elderly individuals. Specific protein 1 (SP1) is involved in OP progression. However, the mechanism by which SP1 regulates OP progression remains unclear.

objectiveThis study investigated the mechanism underlying the function of SP1 in OP.

methodsSAMP6 mice were used to establish an in vivo model of age-dependent OP, and BALB/c mice were used as controls. BMSCs were extracted from two subtypes of mice. Hematoxylin and eosin staining were performed to mark the intramedullary trabecular bone structure to evaluate histological changes. ChIP assay was used to assess the targeted regulation between SP1 and miR-133a-3p. The binding sites between MAPK3 and miR-133a-3p were verified using a dual-luciferase reporter assay. The mRNA levels of miR-133a-3p and MAPK3 were detected using quantitative reverse transcription polymerase chain reaction (RT-qPCR). The protein expression of SP1, MAPK3, Colla1, OCN, and Runx2 was examined using Western blotting. Alkaline phosphatase (ALP) kit and Alizarin Red S staining were used to investigate ALP activity and mineralized nodules, respectively.

resultsThe levels of SP1 and miR-133a-3p were upregulated, whereas the expression of MAPK3 was downregulated in BMSCs from SAMP6 mice, and miR-133a-3p inhibitor accelerated osteogenic differentiation in BMSCs. SP1 directly targeted miR-133a-3p, and MAPK3 was the downstream mRNA of miR-133a-3p. Mechanically, SP1 accelerated osteogenic differentiation in BMSCs via transcriptional mediation of the miR-133a-3p/MAPK3 axis.

conclusionSP1 regulates osteogenic differentiation by mediating the miR-133a-3p/MAPK3 axis, which would shed new light on strategies for treating senile OP.

Indexed as

Cell DifferentiationMesenchymal Stem CellsMicroRNAsMitogen-Activated Protein Kinase 3OsteogenesisOsteoporosisSp1 Transcription FactorAnimalsCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred BALB CMapk3 protein, mouseMicroRNAsMirn133 microRNA, mouseMitogen-Activated Protein Kinase 3Sp1 Transcription FactorBMSCsMAPK3MiR-133a-3pOsteoporosisSP1

Identifiers

PMID38982418
PMCPMC11232211

What OpenQuestion holds

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LicenceCC BY
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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.