Evidence map›Paper›PMID 33906607›Full record

ArticleBMC molecular and cell biology2021

Uncarboxylated osteocalcin alleviates the inhibitory effect of high glucose on osteogenic differentiation of mouse bone marrow-derived mesenchymal stem cells by regulating TP63.

Fangzi Gong, Le Gao, Luyao Ma, Guangxin Li, Jianhong Yang

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

Article in BMC molecular and cell biology, 2021. 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
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 16 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

5 authors at 2 institutions in 1 country.

Fangzi GongMedical School, University of Chinese Academy of Sciences, Beijing, China.
Le GaoMedical School, University of Chinese Academy of Sciences, Beijing, China.
Luyao MaMedical School, University of Chinese Academy of Sciences, Beijing, China.
Guangxin LiCollege of sports medicine and physical therapy, Beijing Sport University, Beijing, China.
Jianhong YangMedical School, University of Chinese Academy of Sciences, Beijing, China. yangjh@ucas.edu.cn.
University of Chinese Academy of Sciences · CNBeijing Sport University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgressive population aging has contributed to the increased global prevalence of diabetes and osteoporosis. Inhibition of osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by hyperglycemia is a potential pathogenetic mechanism of osteoporosis in diabetic patients. Uncarboxylated osteocalcin (GluOC), a protein secreted by mature osteoblasts, regulates bone development as well as glucose and lipid metabolism. In our previous studies, GluOC was shown to promote osteoblastic differentiation of BMSCs; however, the underlying mechanisms are not well characterized. Tumor protein 63 (TP63), as a  transcription factor, is closely related to bone development and glucose metabolism.

resultsIn this study, we verified that high glucose suppressed osteogenesis and upregulated adipogenesis in BMSCs, while GluOC alleviated this phenomenon. In addition, high glucose enhanced TP63 expression while GluOC diminished it. Knock-down of TP63 by siRNA transfection restored the inhibitory effect of high glucose on osteogenic differentiation. Furthermore, we detected the downstream signaling pathway PTEN/Akt/GSK3β. We found that diminishing TP63 decreased PTEN expression and promoted the phosphorylation of Akt and GSK3β. We then applied the activator and inhibitor of Akt, and concluded that PTEN/Akt/GSK3β participated in regulating the differentiation of BMSCs.

conclusionsOur results indicate that GluOC reduces the inhibitory effect of high glucose on osteoblast differentiation by regulating the TP63/PTEN/Akt/GSK3β pathway. TP63 is a potential novel target for the prevention and treatment of diabetic osteoporosis.

Indexed as

OsteogenesisAdipogenesisAnimalsBone Marrow CellsCell DifferentiationGlucoseMesenchymal Stem CellsMiceOsteocalcinSignal TransductionTrans-ActivatorsGlucoseOsteocalcinTrans-ActivatorsTrp63 protein, mouseBone marrow mesenchymal stem cellHigh glucoseOsteogenesisTP63Uncarboxylated osteocalcin

Identifiers

PMID33906607
PMCPMC8080387
OpenAlexW3158237258

What OpenQuestion holds

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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.