Evidence map›Paper›PMID 31358051›Full record

ArticleStem cell research & therapy2019

Mouse embryonic palatal mesenchymal cells maintain stemness through the PTEN-Akt-mTOR autophagic pathway.

Lungang Shi, Binchen Li, Binna Zhang, Congyuan Zhen, Jianda Zhou, Shijie Tang

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 25 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 4 institutions in 1 country.

Lungang ShiDepartment of Plastic Surgery and Burn Center, the Second Affiliated Hospital of Shantou University Medical College, North Dongxia Road, Shantou, 515041, Guangdong, China.
Binchen LiShantou University Medical College, No. 22 Xinling road, Shantou, 515041, Guangdong, China.
Binna ZhangCenter for Translational Medicine, the Second Affiliated Hospital of Shantou University Medical College, North Dongxia Road, Shantou, 515041, Guangdong, China.
Congyuan ZhenShantou University Medical College, No. 22 Xinling road, Shantou, 515041, Guangdong, China.
Jianda ZhouDepartment of Plastic Surgery, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Shijie TangDepartment of Plastic Surgery and Burn Center, the Second Affiliated Hospital of Shantou University Medical College, North Dongxia Road, Shantou, 515041, Guangdong, China. SJtang3@stu.edu.cn.
Second Affiliated Hospital of Shantou University Medical College · CNShantou University · CNShantou University Medical College · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth genetic and environmental factors are implicated in the pathogenesis of cleft palate. However, the molecular and cellular mechanisms that regulate the development of palatal shelves, which are composed of mesenchymal cells, have not yet been fully elucidated. This study aimed to determine the stemness and multilineage differentiation potential of mouse embryonic palatal mesenchyme (MEPM) cells in palatal shelves and to explore the underlying regulatory mechanism associated with cleft palate formation.

methodsPalatal shelves excised from mice models were cultured in vitro to ascertain whether MEPM are stem cells through immunofluorescence and flow cytometry. The osteogenic, adipogenic, and chondrogenic differentiation potential of MEPM cells were also determined to characterize MEPM stemness. In addition, the role of the PTEN-Akt-mTOR autophagic pathway was investigated using quantitative RT-PCR, Western blotting, and transmission electron microscopy.

resultsMEPM cells in culture exhibited cell surface marker expression profiles similar to that of mouse bone marrow stem cells and exhibited positive staining for vimentin (mesodermal marker), nestin (ectodermal marker), PDGFRα, Efnb1, Osr2, and Meox2 (MEPM cells markers). In addition, exposure to PDGFA stimulated chemotaxis of MEPM cells. MEPM cells exhibited stronger potential for osteogenic differentiation as compared to that for adipogenic and chondrogenic differentiation. Undifferentiated MEPM cells displayed a high concentration of autophagosomes, which disappeared after differentiation (at passage four), indicating the involvement of PTEN-Akt-mTOR signaling.

conclusionsOur findings suggest that MEPM cells are ectomesenchymal stem cells with a strong osteogenic differentiation potential and that maintenance of their stemness via PTEN/AKT/mTOR autophagic signaling prevents cleft palate development.

Indexed as

AnimalsAutophagyCell DifferentiationFemaleMaleMesenchymal Stem CellsMiceOsteogenesisPalateProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTOR Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTOR Serine-Threonine KinasesAutophagyMouse embryonic palatal mesenchyme cellsPTEN-Akt-mTOR signaling pathwayStemness

Identifiers

PMID31358051
PMCPMC6664599
OpenAlexW2965190935

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.