ArticleBioscience reports2020
Per2 attenuates LPS-induced chondrocyte injury through the PTEN/PI3K/Akt signalling pathway.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- DJ-1 promotes necroptosis of chondrocytes by the PTEN/PI3K-AKT signaling pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Mesenchymal stem cell-derived extracellular vesicles ameliorate heat stroke-induced hippocampal injury and modulate VIM-AS1-associated miR-34a-5p/Per2 signaling.Frontiers in immunology · 2026Article
- Circadian Period 2 (Per2) downregulate inhibitor of differentiation 3 (Id3) expression via PTEN/AKT/Smad5 axis to inhibits glioma cell proliferation.Bioengineered · 2022Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This research aimed to explore the role of period circadian clock 2 (Per2) in the evolution of osteoarthritis (OA) and the relevant mechanisms. Per2 messenger RNA (mRNA) and protein levels were markedly reduced in NHAC-kn cells treated with 5 µg/ml lipopolysaccharide (LPS) for 12 h. Then, pcDNA3.1-Per2 and si-Per2 were recruited to boost and reduce the expression of Per2, respectively. MTT assay, apoptosis analysis and enzyme-linked immunosorbent assay (ELISA) results showed that Per2 increased cell proliferation, while inhibited apoptosis and inflammation. Furthermore, the PTEN/PI3K/Akt signalling pathway was activated by Per2 overexpression; the CO-IP data confirmed that Per2 specifically bound to PTEN. Through employing IGF-1, a PI3K activator, we determined that Per2-mediated inflammation response in LPS-stimulated NHAC-kn cells through the PTEN/PI3K/Akt signalling pathway. In summary, the present study indicates that Per2 may serve as a novel therapeutic target through activating the PTEN/PI3K/Akt signalling pathway.
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Registered trials
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.