ArticleCell death discovery2018
Cell cycle shift from G0/G1 to S and G2/M phases is responsible for increased adhesion of calcium oxalate crystals on repairing renal tubular cells at injured site.
Article in Cell death discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Unveiling potential natural promoters of calcium oxalate kidney stones in the urine via anion-exchange chromatography, crystal assays, and proteomics.Molecular and cellular biochemistry · 2026Article
- Lactobacillus acidophilus abolishes oxalate-mediated renal epithelial barrier disruption and calcium oxalate monohydrate crystal adhesion to renal epithelial cells.Cellular & molecular biology letters · 2026Article
- Methylated 1,2-naphthoquinone derivative SJ006 as an inhibitor of human glucose 6-phosphate dehydrogenase in non-small cell lung cancer cell lines.Scientific reports · 2025Article
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- Effect of Drying Methods on the Phenolic Profile and Antioxidant Capacity ofMolecules (Basel, Switzerland) · 2025Article
- Cyclosporine A Causes Gingival Overgrowth by Promoting Entry into the S Phase at the G1/S Cell Cycle Checkpoint in Gingival Fibroblasts Exposed to Lipopolysaccharide.Diseases (Basel, Switzerland) · 2024Article
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- SMYD2 Promotes Calcium Oxalate-Induced Glycolysis in Renal Tubular Epithelial Cells via PTEN Methylation.Biomedicines · 2024Article
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- Silver ciprofloxacin (CIPAG): a multitargeted metallodrug in the development of breast cancer therapy.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024Article
- Cyclosporine A causes gingival overgrowth via reduced G1 cell cycle arrest in gingival fibroblasts.PloS one · 2024Article
- Resveratrol inhibits calcium oxalate crystal growth, reduces adhesion to renal cells and induces crystal internalization into the cells, but promotes crystal aggregation.Current research in food science · 2024Article
- Mitochondria-derived vesicles and their potential roles in kidney stone disease.Journal of translational medicine · 2023Review
- Proteomic and computational analyses followed by functional validation of protective effects of trigonelline against calcium oxalate-induced renal cell deteriorations.Computational and structural biotechnology journal · 2023Article
- Caffeine causes cell cycle arrest at G0/G1 and increases of ubiquitinated proteins, ATP and mitochondrial membrane potential in renal cells.Computational and structural biotechnology journal · 2023Article
- Characterizations of annexin A1-interacting proteins in apical membrane and cytosolic compartments of renal tubular epithelial cells.Computational and structural biotechnology journal · 2023Article
- Assay-ready Cryopreserved Cell Monolayers Enabled by Macromolecular Cryoprotectants.Biomacromolecules · 2022Article
- Effects of alternative splicing events and transcriptome changes on kidney stone formation.Urolithiasis · 2022Article
- The Effect of Proinflammatory Cytokines on the Proliferation, Migration and Secretory Activity of Mesenchymal Stem/Stromal Cells (WJ-MSCs) under 5% OJournal of clinical medicine · 2021Article
- Wound Healing Activity of a Novel Formulation SKRIN via Induction of Cell Cycle Progression and Inhibition of PCNA-p21 Complex Interaction Leading to Cell Survival and Proliferation.ACS pharmacology & translational science · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubular cell injury can enhance calcium oxalate monohydrate (COM) crystal adhesion at the injured site and thus may increase the stone risk. Nevertheless, underlying mechanism of such enhancement remained unclear. In the present study, confluent MDCK renal tubular cell monolayers were scratched to allow cells to proliferate and repair the injured site. At 12-h post-scratch, the repairing cells had significant increases in crystal adhesion capacity and cell proliferation as compared to the control. Cell cycle analysis using flow cytometry demonstrated that the repairing cells underwent cell cycle shift from G0/G1 to S and G2/M phases. Cyclosporin A (CsA) and hydroxyurea (HU) at sub-toxic doses caused cell cycle shift mimicking that observed in the repairing cells. Crystal-cell adhesion assay confirmed the increased crystal adhesion capacity of the CsA-treated and HU-treated cells similar to that of the repairing cells. These findings provide evidence indicating that cell cycle shift from G0/G1 to S and G2/M phases is responsible, at least in part, for the increased adhesion of COM crystals on repairing renal tubular cells at the injured site.
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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.