Evidence map›Paper›PMID 37340717›Full record

ArticleThe Journal of international medical research2023

Activation of the mTOR pathway promotes neurite growth through upregulation of CD44 expression.

Jiwei Zhang, Wenjuan Gan, Ru Peng, Lei Lu, Weiqing Lu, Jiamei Liu

Open access · goldAbstract read
In one paragraph

Article in The Journal of international medical research, 2023. 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
0.8field-weighted citation impact, top 27% 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, 5 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.

Jiwei ZhangDepartment of Pathology, Dushu Lake Hospital Affiliated to Soochow University, Suzhou, Jiangsu, 215123, China.ORCID 0000-0002-1658-7390
Wenjuan GanDepartment of Pathology, Dushu Lake Hospital Affiliated to Soochow University, Suzhou, Jiangsu, 215123, China.
Ru PengDepartment of Histology and Embryology College of Basic Medical Sciences, Jilin University, No. 828, Xinmin Road Changchun 130061, China.
Lei LuCollaborative Innovation Center of Suzhou Nano Science and Technology, Soochow University, Suzhou 215021, China.
Weiqing LuDepartment of Pathology, Dushu Lake Hospital Affiliated to Soochow University, Suzhou, Jiangsu, 215123, China.
Jiamei LiuDepartment of Histology and Embryology College of Basic Medical Sciences, Jilin University, No. 828, Xinmin Road Changchun 130061, China.
Soochow University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the intrinsic mechanism of the mammalian target of rapamycin (mTOR) pathway activation and promotion of neuronal axon growth.

methodsHuman neuroblastoma cells, SH-SY5Y, were induced with all-trans retinoic acid (ATRA; 10 μM for three days) which differentiated the cell line into a neuronal-like state. Immunohistochemical staining was used to detect the differentiation status of the neuronal-like cells. Phosphatase and tensin homolog (PTEN) RNA interference (RNAi) experiments were performed on the differentiated cells; reverse transcription-polymerase chain reaction (RT-PCR) detected transcriptional levels of PTEN following 24 h of interference. After 36 h, western blot assay was used to detect expression levels of ribosomal protein S6 kinase (pS6k) and mTOR. To downregulate the expression of PTEN and cluster of differentiation 44 (CD44), a cell-surface glycoprotein, simultaneously, PTEN siRNA and CD44 siRNA sequences were mixed in equal proportions in co-interference experiments. RT-PCR detected the transcription level of CD44, and the relationship between the CD44 and axonal growth was observed after 48 h of interference.

resultsMicrotubule-associated protein 2 (MAP2) expression was enhanced after three days of induction in SH-SY5Y cells. RT-PCR showed the transcription level of PTEN was significantly downregulated after 24 h of PTEN knockdown. mTOR and pS6k protein expression levels were significantly upregulated after 36 h of interference. CD44 transcription levels were upregulated after PTEN gene interference. The neurite length of the cells in the experimental interference group was significantly longer than that in the control group, and the expression level of CD44 was positively correlated with neurite growth. The neurite length of the PTEN-only interference group was significantly greater than that of the co-interference and ATRA groups.

conclusionActivation of the mTOR pathway promoted neurite growth through upregulation of CD44 expression, thus promoting neuronal regeneration.

Indexed as

NeuritesNeuroblastomaHumansHyaluronan ReceptorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, Small InterferingSirolimusTOR Serine-Threonine KinasesUp-RegulationCD44 protein, humanHyaluronan ReceptorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, Small InterferingSirolimusTOR Serine-Threonine KinasesAxonal growthCD44mTOR pathwayNerve regeneration

Identifiers

PMID37340717
PMCPMC10288410
OpenAlexW4381470589

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.