Evidence map›Paper›PMID 34307680›Full record

ArticleBioMed research international2021

Role of PI3K/AKT Signaling Pathway in Nucleus Pulposus Cells.

Quan Xiao, Yun Teng, Changming Xu, Wei Pan, Hanshi Yang, Jiali Zhao, Quan Zhou

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

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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

5 citing papers in PubMed, 7 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

7 authors at 3 institutions in 1 country.

Quan XiaoDepartment of Orthopaedic Surgery, The Affiliated Lianshui People's Hospital of Kangda College of Nanjing Medical Universty, Lianshui, Jiangsu, China.
Yun TengDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Changming XuDepartment of Orthopaedic Surgery, The Affiliated Lianshui People's Hospital of Kangda College of Nanjing Medical Universty, Lianshui, Jiangsu, China.
Wei PanDepartment of Orthopaedic Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu 223002, China.
Hanshi YangDepartment of Orthopaedic Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu 223002, China.
Jiali ZhaoDepartment of Orthopaedic Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu 223002, China.
Quan ZhouDepartment of Orthopaedic Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu 223002, China.ORCID https://orcid.org/0000-0002-9619-2187
Xuzhou Medical College · CNKangda College of Nanjing Medical UniversitySoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role of PI3K/AKT signaling pathway in nucleus pulposus (NP) cells.

methodsNucleus pulposus (NP) cells were isolated from SD rat, and thereafter, passage three (P3) NP cells were divided into the following experimental groups: control, PI3K/AKT agonist IGF-1 (25 ng/ml, 50 ng/ml, and 100 ng/ml), and PI3K/AKT inhibitor LY294002 (5

resultsPI3K/AKT inhibitor LY294002 increased the rate of apoptosis in NP cells when compared to the control and decreased the proliferation rate when compared to control. Moreover, LY294002 decreased the protein expression level of Col-II and Aggrecan in NP cells. At the same time, LY294002 increased the protein expression level of MMP13 and Col-X in NP cells. Through activating PI3K/AKT, IGF-1 increased the proliferation rate when compared to control and decreased the rate of apoptosis when compared to control. Additionally, IGF-1 decreased the protein expression level of MMP13 and Col-X and increased Col-II and Aggrecan in NP cells.

conclusionThe inhibition of PI3K/AKT signaling pathway accelerated the apoptosis of NP cells and facilitated the extracellular matrix degradation. However, the activation of PI3K/AKT pathway partly prevented the NP cell from apoptosis and promoted their proliferation. Meanwhile, its activation also delayed the loss of extracellular matrix.

Indexed as

Signal TransductionAnimalsApoptosisCell ProliferationChromonesInsulin-Like Growth Factor IMorpholinesNucleus PulposusPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRatsRats, Sprague-Dawley2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesInsulin-Like Growth Factor IMorpholinesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID34307680
PMCPMC8270693
OpenAlexW3175725782

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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.