ArticleThe Journal of cell biology1994
Autocrine signals enable chondrocytes to survive in culture.
Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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
17 citing papers in PubMed, 131 citations in OpenAlex.
- The Dual-Responsive Interaction of Particulated Hyaline Cartilage and Plasma Rich in Growth Factors (PRGF) in the Repair of Cartilage Defects: An In Vitro Study.International journal of molecular sciences · 2023Article
- Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis.International journal of molecular sciences · 2015Review
- Peripheral blood derived mononuclear cells enhance osteoarthritic human chondrocyte migration.Arthritis research & therapy · 2015Article
- CD44-positive cells are candidates for astrocyte precursor cells in developing mouse cerebellum.Cerebellum (London, England) · 2012Article
- Cell death in osteoarthritis.Current rheumatology reports · 2008Review
- Chondrocyte cell death mediated by reactive oxygen species-dependent activation of PKC-betaI.American journal of physiology. Cell physiology · 2006Article
- Cartilage and bone tissue engineering for reconstructive head and neck surgery.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2005Review
- Prologation of c-Jun N-terminal kinase is associated with cell death induced by tumor necrosis factor alpha in human chondrocytes.Journal of Korean medical science · 2004Article
- Low-density induced apoptosis of cortical neurons is inhibited by serum factors.Cellular and molecular neurobiology · 1998Article
- Bcl-2 lies downstream of parathyroid hormone-related peptide in a signaling pathway that regulates chondrocyte maturation during skeletal development.The Journal of cell biology · 1997Article
- Glucose promotes survival of rat pancreatic beta cells by activating synthesis of proteins which suppress a constitutive apoptotic program.The Journal of clinical investigation · 1996Article
- Nerve growth factor (NGF)-mediated protection of neural crest cells from antimitotic agent-induced apoptosis: the role of the low-affinity NGF receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996Article
- Constitutive expression of the machinery for programmed cell death.The Journal of cell biology · 1996Article
- Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death.The Journal of cell biology · 1996Article
- Retinoic acid modulation of glutathione and cysteine metabolism in chondrocytes.The Biochemical journal · 1996Article
- Programmed cell death by default in embryonic cells, fibroblasts, and cancer cells.Molecular biology of the cell · 1995Article
- Nucleolar localization of parathyroid hormone-related peptide enhances survival of chondrocytes under conditions that promote apoptotic cell death.Molecular and cellular biology · 1995Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently proposed that most mammalian cells other than blastomeres may be programmed to kill themselves unless continuously signaled by other cells not to. Many observations indicate that some mammalian cells are programmed in this way, but is it the case for most mammalian cells? As it is impractical to test all of the hundreds of types of mammalian cells, we have focused on two tissues--lens and cartilage--which each contain only a single cell type: if there are cells that do not require signals from other cells to avoid programmed cell death (PCD), lens epithelial cells and cartilage cells (chondrocytes) might be expected to be among them. We have previously shown that rat lens epithelial cells can survive in serum-free culture without signals from other cell types but seem to require signals from other lens epithelial cells to survive: without such signals they undergo PCD. We show here that the same is true for rat (and chick) chondrocytes. They can survive for weeks in culture at high cell density in the absence of other cell types, serum, or exogenous proteins or signaling molecules, but they die with the morphological features of apoptosis in these conditions at low cell density. Medium from high density cultures, FCS, or a combination of known growth factors, all support prolonged chondrocyte survival in low density cultures, as long as antioxidants are also present. Moreover, medium from high density chondrocyte cultures promotes the survival of lens epithelial cells in low density cultures and vice versa. Chondrocytes isolated from adult rats behave similarly to those isolated from developing rats. These findings support the hypothesis that most mammalian cells require signals from other cells to avoid PCD, although the signals can sometimes be provided by cells of the same type, at least in tissues that contain only one cell type.
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Registered trials
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