ArticleAmerican journal of physiology. Cell physiology2006
Chondrocyte cell death mediated by reactive oxygen species-dependent activation of PKC-betaI.
Article in American journal of physiology. Cell physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Cellular and Molecular Responses to Mitochondrial DNA Deletions in Kearns-Sayre Syndrome: Some Underlying Mechanisms.Molecular neurobiology · 2024Review
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
- Interplay between Protein Kinase C Epsilon and Reactive Oxygen Species during Myogenic Differentiation.Cells · 2023Article
- Injectable Hyaluronan-Based Thermoresponsive Hydrogels for Dermatological Applications.Pharmaceutics · 2023Article
- Natural compounds protect against the pathogenesis of osteoarthritis by mediating the NRF2/ARE signaling.Frontiers in pharmacology · 2023Review
- Iron Overload Induces Oxidative Stress, Cell Cycle Arrest and Apoptosis in Chondrocytes.Frontiers in cell and developmental biology · 2022Article
- Polylysine for skin regeneration: A review of recent advances and future perspectives.Bioengineering & translational medicine · 2022Review
- Mitochondria Lead the Way: Mitochondrial Dynamics and Function in Cellular Movements in Development and Disease.Frontiers in cell and developmental biology · 2021Review
- Alterations in the chondrocyte surfaceome in response to pro-inflammatory cytokines.BMC molecular and cell biology · 2020Article
- Reactive oxygen species, aging and articular cartilage homeostasis.Free radical biology & medicine · 2019Review
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
- Cell Death in Chondrocytes, Osteoblasts, and Osteocytes.International journal of molecular sciences · 2016Review
- Cross-talk between NADPH oxidase-PKCα-p(38)MAPK and NF-κB-MT1MMP in activating proMMP-2 by ET-1 in pulmonary artery smooth muscle cells.Molecular and cellular biochemistry · 2016Article
- Mitochondrial respiration and redox coupling in articular chondrocytes.Arthritis research & therapy · 2015Article
- Clostridium perfringens phospholipase C induced ROS production and cytotoxicity require PKC, MEK1 and NFκB activation.PloS one · 2014Article
- Vitamin E protects chondrocytes against hydrogen peroxide-induced oxidative stress in vitro.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- Kearns-Sayre syndrome presenting as isolated growth failure.BMJ case reports · 2013Article
- PKCε signalling activates ERK1/2, and regulates aggrecan, ADAMTS5, and miR377 gene expression in human nucleus pulposus cells.PloS one · 2013Article
- Article
- Cell signaling through protein kinase C oxidation and activation.International journal of molecular sciences · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Signals generated by the extracellular matrix (ECM) promote cell survival. We have shown that chondrocytes detached from their native ECM and plated without serum at low density on poly-l-lysine undergo significant cell death that is associated with the production of reactive oxygen species (ROS). No cell death or ROS production was observed when cells were plated on fibronectin under the same conditions. Cell death on poly-l-lysine could be completely inhibited with the addition of either antioxidants or inhibitors of specific protein kinase C (PKC) isoforms including PKC-betaI. PKC-betaI was noted to translocate from the cytosol to the particulate membrane after plating on poly-l-lysine, and this translocation was inhibited by the addition of an antioxidant. Time-course analyses implicated endogenous ROS production as a secondary messenger leading to PKC-betaI activation and subsequent chondrocyte cell death. Cell survival on poly-l-lysine was significantly improved in the presence of oligomycin or DIDS, suggesting that ROS production occurred via complex V of the electron transport chain of the mitochondria and that ROS were released to the cytosol via voltage-dependent anion channels. Together, these results represent a novel mechanism by which ROS can initiate cell death through the activation of PKC-betaI.
Indexed as
Identifiers
What OpenQuestion holds
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.