Evidence map›Paper›PMID 29890823›Full record

ArticleMolecules and cells2018

TNF-α-Induced SOX5 Upregulation Is Involved in the Osteogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells Through KLF4 Signal Pathway.

Lijun Xu, Lili Zheng, Zhifang Wang, Chong Li, Shan Li, Xuedi Xia, Pengyan Zhang, Li Li, Lixia Zhang

Abstract read
In one paragraph

Article in Molecules and cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Role of SOX Transcription Factors in Ageing and Age-Related Diseases.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. [Research progress on mechanism of myokines regulating bone tissue cells].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2021
    Review
  13. Article
  14. Article
  15. 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.

Lijun XuDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Lili ZhengDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Zhifang WangDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Chong LiDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Shan LiDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Xuedi XiaDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Pengyan ZhangDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Li LiDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Lixia ZhangDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postmenopausal osteoporosis (PMOP) is a common systemic skeletal disease characterized by reduced bone mass and microarchitecture deterioration. Although differentially expressed SOX5 has been found in bone marrow from ovariectomized mice, its role in osteogenic differentiation in human mesenchymal stem cells (hMSCs) from bone marrow in PMOP remains unknown. In this study, we investigated the biological function of SOX5 and explore its molecular mechanism in hMSCs from patients with PMOP. Our findings showed that the mRNA and protein expression levels of SOX5 were upregulated in hMSCs isolated from bone marrow samples of PMOP patients. We also found that SOX5 overexpression decreased the alkaline phosphatase (ALP) activity and the gene expression of osteoblast markers including Collagen I, Runx2 and Osterix, which were increased by SOX5 knockdown using RNA interference. Furthermore, TNF-α notably upregulated the SOX5 mRNA expression level, and SOX5 knockdown reversed the effect of TNF-α on osteogenic differentiation of hMSCs. In addition, SOX5 overexpression increased Kruppel-like factor 4 (KLF4) gene expression, which was decreased by SOX5 silencing. KLF4 knockdown abrogated the suppressive effect of SOX5 overexpression on osteogenic differentiation of hMSCs. Taken together, our results indicated that TNF-α-induced SOX5 upregulation inhibited osteogenic differentiation of hMSCs through KLF4 signal pathway, suggesting that SOX5 might be a novel therapeutic target for PMOP treatment.

Indexed as

AnimalsBone Marrow CellsCase-Control StudiesCell DifferentiationFemaleGene ExpressionHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMesenchymal Stem CellsMiceMiddle AgedOsteoporosis, PostmenopausalRNA, MessengerSignal TransductionSOXD Transcription FactorsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRNA, MessengerSOX5 protein, humanSOXD Transcription FactorsTumor Necrosis Factor-alphahuman mesenchymal stem cellsKLF4osteogenic differentiationpostmenopausal osteoporosisSOX5

Identifiers

PMID29890823
PMCPMC6030245

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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.