ArticleInternational journal of molecular medicine2017
Silencing of both ATF4 and PERK inhibits cell cycle progression and promotes the apoptosis of differentiating chondrocytes.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
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- Endoplasmic Reticulum Stress in Gliomas: Exploiting a Dual-Effect Dysfunction through Chemical Pharmaceutical Compounds and Natural Derivatives for Therapeutical Uses.International journal of molecular sciences · 2024Review
- A stay of execution: ATF4 regulation and potential outcomes for the integrated stress response.Frontiers in molecular neuroscience · 2023Review
- Protein Quality Control in Glioblastoma: A Review of the Current Literature with New Perspectives on Therapeutic Targets.International journal of molecular sciences · 2022Review
- A mitochondria-targeted caffeic acid derivative reverts cellular and mitochondrial defects in human skin fibroblasts from male sporadic Parkinson's disease patients.Redox biology · 2021Article
- Pharmacological Disruption of Phosphorylated Eukaryotic Initiation Factor-2α/Activating Transcription Factor 4/Indian Hedgehog Protects Intervertebral Disc Degeneration via Reducing the Reactive Oxygen Species and Apoptosis of Nucleus Pulposus Cells.Frontiers in cell and developmental biology · 2021Article
- High ATF4 Expression Is Associated With Poor Prognosis, Amino Acid Metabolism, and Autophagy in Gastric Cancer.Frontiers in oncology · 2021Article
- PERK Overexpression-Mediated Nrf2/HO-1 Pathway Alleviates Hypoxia/Reoxygenation-Induced Injury in Neonatal Murine Cardiomyocytes via Improving Endoplasmic Reticulum Stress.BioMed research international · 2020Article
- ATG5 and ATG7 induced autophagy interplays with UPR via PERK signaling.Cell communication and signaling : CCS · 2019Article
- Endoplasmic reticulum stress signalling - from basic mechanisms to clinical applications.The FEBS journal · 2019Review
- Hypophosphatemia Regulates Molecular Mechanisms of Circadian Rhythm.Scientific reports · 2018Article
- Coordinated targeting of MMP-2/MMP-9 by miR-296-3p/FOXCUT exerts tumor-suppressing effects in choroidal malignant melanoma.Molecular and cellular biochemistry · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the current study, we demonstrate that the silencing of protein kinase R (PKR)-like endoplasmic reticulum (ER) kinase (PERK) and activating transcription factor 6 (ATF4) (using small interfering RNA expression constructs) inhibits the chondrocyte cell cycle and proliferation in vitro and ex vivo. The silencing of PERK alone using siRNA against PERK (siPERK) led to arrest in the G1 phase, it decreased the number of cells in the S phase, and delayed progressoin to the G2‑M phase. Co-transfection with siRNA against ATF (siATF4) led to a more profound inhibitory effect on cell cycle progression. Moreover, transfection with siPERK was associated with enhanced endoplasmic reticulum (ER) stress‑induced apoptosis during bone morphogenetic protein 2 (BMP2)‑induced chondrogenesis, and transfection with siATF4 exacerbated ER stress‑related cell death. Data from flow cytometry (FCM), immunohistochemistry and TUNEL assays supported these findings in vitro and ex vivo. As shown by our results, the combined effect of the silencing of ATF4 and PERK led to the activation of an ER stress‑specific caspase cascade in the cartilage tissue. On the whole, these findings reveal a new crucial combined effect of the silencing of PERK and ATF4 in modulating ER stress‑mediated apoptosis during chondrocyte differentiation and proliferation.
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