ArticleBioscience reports2018
Silencing SUMO2 promotes protection against degradation and apoptosis of nucleus pulposus cells through p53 signaling pathway in intervertebral disc degeneration.
Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- MicroRNA-140-3p alleviates intervertebral disc degenerationRNA biology · 2021Article
- SUMOylation modification-mediated cell death.Open biology · 2021Review
- MicroRNA-199a-5p accelerates nucleus pulposus cell apoptosis and IVDD by inhibiting SIRT1-mediated deacetylation of p21.Molecular therapy. Nucleic acids · 2021Article
- SUMO modification in apoptosis.Journal of molecular histology · 2021Review
- Hub Genes and Key Pathways of Intervertebral Disc Degeneration: Bioinformatics Analysis and Validation.BioMed research international · 2021Article
- Moderate hypothermia induces protection against hypoxia/reoxygenation injury by enhancing SUMOylation in cardiomyocytes.Molecular medicine reports · 2020Article
- Effects of the NF‑κB/p53 signaling pathway on intervertebral disc nucleus pulposus degeneration.Molecular medicine reports · 2020Article
- Knockdown of hsa_circ_0059955 Induces Apoptosis and Cell Cycle Arrest in Nucleus Pulposus Cells via InhibitingDrug design, development and therapy · 2020Article
- Syndecan-4 is a Novel Therapeutic Target for Intervertebral Disc Degeneration via Suppressing JNK/p53 Pathway.International journal of biological sciences · 2020Article
- miRNA-141 Induced Pyroptosis in Intervertebral Disk Degeneration by Targeting ROS Generation and Activating TXNIP/NLRP3 Signaling in Nucleus Pulpous Cells.Frontiers in cell and developmental biology · 2020Article
- Molecular basis of degenerative spinal disorders from a proteomic perspective (Review).Molecular medicine reports · 2020Article
Corrections and comments
- Retraction · 2021-10-05Duplication of/in Image · Investigation by Third Party · Paper Mill · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/4C430E87579F36FDBD35EE20138094 and https://scienceintegritydigest.com/2020/02/21/the-tadpole-paper-mill/
- Expression of concern · 2020-08-28Concerns/Issues about Image · Investigation by Third Party · Paper Mill · Updated to Retraction · · see also: https://pubpeer.com/publications/4C430E87579F36FDBD35EE20138094 and https://scienceintegritydigest.com/2020/02/21/the-tadpole-paper-mill/
- Expression of concern
- Retracted
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIntervertebral disc degeneration (IDD), as a common cause of back pain, is related to the promotion of cellular senescence and reduction in proliferation. Based on recent studies, small ubiquitin-related modifier (SUMO) proteins have been implicated in various biological functions. Therefore, in the present study, we investigated the effects of SUMO2 on proliferation and senescence of nucleus pulposus cells (NPCs) via mediation of p53 signaling pathway in rat models of IDD.
methodsAfter the establishment of rat models of IDD for the measurement of positive expression of SUMO2/3 protein, the mRNA and protein levels of SUMO2, molecular phenotype [matrix metalloproteinase-2 (MMP-2) and hypoxia-inducible factor-1α (HIF-1α)] and p53 signaling pathway-related genes [p21, murine double minute-2 (MDM2), growth arrest and DNA-damage-inducible protein 45 α (GADD45α), cyclin-dependent kinase 2/4 (CDK2/4), and CyclinB1] were determined, followed by the detection of cell proliferation, cell cycle, apoptosis, and cell senescence.
resultsThe rat models of IDD were successfully constructed. The results obtained showed that there was a higher positive expression of SUMO2/3 protein in IDD rats. Moreover, the silencing of the SUMO2 gene decreases the levels of SUMO2, p53, p21, MDM2, GADD45α, MMP-2, and HIF-1α expressions and p53 phosphorylation level while it increases the levels of CDK2/4 and CyclinB1 expressions. In addition, SUMO2 gene silencing enhances proliferation and suppresses apoptosis and cell senescence of NPCs.
conclusionIn conclusion, SUMO2 gene silencing promotes proliferation, and inhibits the apoptosis and senescence of NPCs in rats with IDD through the down-regulation of the p53 signaling pathway. Thus, SUMO2 is a potential target in the treatment of IDD.
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