Evidence map›Paper›PMID 33823913›Full record

ArticleStem cell research & therapy2021

GSK3β rephosphorylation rescues ALPL deficiency-induced impairment of odontoblastic differentiation of DPSCs.

Liqiang Zhang, Jiangdong Zhao, Jiayi Dong, Yuting Liu, Kun Xuan, Wenjia Liu

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

Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 6 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

6 authors at 2 institutions in 1 country.

Liqiang Zhang *National & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 Xiwu Road, Xi'an, 710004, China.
Jiangdong Zhao *The Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an, 710032, Shaanxi, China.
Jiayi DongState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi International Joint Research Center for Oral Diseases, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, No. 145 West Changle Road, Xi'an, 710032, Shaanxi, China.
Yuting LiuNational & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 Xiwu Road, Xi'an, 710004, China.
Kun XuanState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi International Joint Research Center for Oral Diseases, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, No. 145 West Changle Road, Xi'an, 710032, Shaanxi, China. xuankun@fmmu.edu.cn.
Wenjia LiuNational & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 Xiwu Road, Xi'an, 710004, China. wenjialiu@xjtu.edu.cn.
Air Force Medical University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPremature exfoliation of the deciduous teeth is a common manifestation in childhood patients with hypophosphatasia (HPP), which is an autosomal inherited disease caused by ALPL mutations. Dysplasia of the cementum, dentin, and alveolar bone has been proposed to be the main reasons for the exfoliation of teeth, while the extraordinarily complex intracellular mechanisms remain elusive. Dental pulp stem cells (DPSCs) have been demonstrated to successfully regenerate functional pulp-dentin-like tissue. Dental pulp cells derived from HPP patients impaired mineralization; however, insight into the deeper mechanism is still unclear.

methodsThe effects of ALPL on odontoblastic differentiation of DPSCs from HPP patient were assessed by Alizarin Red staining, immunofluorescent staining, Western blot and RT-PCR, and micro-CT assays.

resultHere, we found DPSCs from HPP patient exhibited low ALP activity and impaired odontoblastic differentiation. Meanwhile, we found that loss of function of ALPL reduced phosphorylation of GSK3β in DPSCs. While GSK3β rephosphorylation improved odontoblastic differentiation of HPP DPSCs with LiCl treatment. Finally, we demonstrated systemic LiCl injection ameliorated tooth-associated defects in ALPL

conclusionsOur study indicates that ALPL regulates odontoblastic differentiation of DPSCs and provides useful information for understanding how ALPL deficiency led to tooth dysplasia and, ultimately, may inform efforts at improvement tooth defects in HPP patients.

Indexed as

Alkaline PhosphataseHypophosphatasiaAnimalsCell DifferentiationDental PulpGlycogen Synthase Kinase 3 betaHumansMiceTooth ExfoliationAlkaline PhosphataseALPL protein, humanGlycogen Synthase Kinase 3 betaALPLDPSCsGSK3βHypophosphatasiaOdontoblastic differentiationTooth defects

Identifiers

PMID33823913
PMCPMC8022410
OpenAlexW3111239936

What OpenQuestion holds

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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.