Murine Bone Marrow-Derived Mast Cells Exhibit Evidence of Both Apoptosis and Oncosis After IL-3 Deprivation

Park, Bong Soo; Kim, Gyoo Cheon; Baek, Soo Jin; Kim, Nam Deuk; Kim, Yang Soon; Kim, Seok Kwon; Jeong, Min Ho; Lim, Young Jin; Yoo, Young Hyun

doi:10.3109/08820130009060877

Cited by 10 publications

(6 citation statements)

References 23 publications

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“…28,29,31 IL-3 can prevent apoptosis in many cell types. 12,13,15 The reason why it takes 48 hr for IL-3 to prevent basophil apoptosis may be a result of the time it takes for IL-3 to induce anti-apoptotic gene expression and protein synthesis. In this study, new RNA and protein synthesis was required for the protection of basophil apoptosis by IL-3, because this process was completely blocked by cycloheximide, a protein synthesis inhibitor, and actinomycin D, an inhibitor of transcription.…”

Section: Discussionmentioning

confidence: 99%

“…It has been known for many years that GM-CSF, IL-5 and IL-3 can inhibit apoptosis in many cell types, including eosinophils, 11,12 mast cells 13 and other haematopoietic cells. 14,15 To determine whether IL-3 and GM-CSF þ IL-5 exhibit the same anti-apoptotic effect in basophils as they do in eosinophils, freshly isolated human basophils and eosinophils were incubated with IL-3 (300 pM) or GM-CSF (10 pM) þ IL-5 (100 pM) for 24, 48 and 72 hr.…”

Section: Il-3 But Not Gm-csf þ Il-5 Inhibits Apoptosis In Human Matmentioning

confidence: 99%

“…Apoptosis is a form of cell death in which the cell participates in its own demise. IL-3, which is derived from T cells and other sources, has been shown to inhibit apoptosis in many cell types, including eosinophils, 11,12 mast cells 13 and other haematopoietic cells. 14,15 IL-3-dependent cell survival of haematopoietic cells is known to rely on the activation of multiple signalling pathways, including a pathway leading to activation of phosphatidylinositol 3-kinase (PI3-K).…”

Section: Introductionmentioning

confidence: 99%

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Interleukin‐3, but not granulocyte–macrophage colony‐stimulating factor and interleukin‐5, inhibits apoptosis of human basophils through phosphatidylinositol 3‐kinase: requirement of NF‐κB‐dependent and ‐independent pathways

et al. 2002

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SUMMARYBasophils are key effector cells of allergic reactions. Although proinflammatory cytokines, such as interleukin (IL)-3, granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-5, inhibit eosinophil apoptosis in vitro, little is known about basophil apoptosis, and the signalling mechanisms required for basophil survival remain undefined. To address this issue, we used a novel negative-selection system to isolate human basophils to a purity of >95%, and evaluated apoptosis by morphology using light and transmission electron microscopy, and by annexin-V binding and propidium iodide incorporation using flow cytometry. In this study, we demonstrated that the spontaneous rate of apoptotic basophils was higher than that of eosinophils as, at 24 hr, 57Á6 AE 4Á7% of basophils underwent apoptosis compared with 39Á5 AE 3Á8% of eosinophils. In addition, basophil cell death was significantly inhibited when cultured with IL-3 for 48 hr (84Á6 AE 4Á9% vehicletreated cells versus 40Á9 AE 3Á9% IL-3-treated cells). IL-3 also up-regulated basophil CD69 surface expression. The effects of IL-3 on apoptosis and CD69 surface expression of human basophils were completely blocked by LY294002 (LY), a potent inhibitor of phosphatidylinositol 3-kinase (PI3-K), but only partially inhibited by lactacystin, a proteasome inhibitor that prevents degradation of IkB and NF-kB translocation. These observations reveal the novel finding that IL-3 prevents basophil apoptosis through the activation of PI3-K, which is only partially NF-kB dependent. As basophils are active participants in allergic reactions and IL-3 is one of the abundant proinflammatory cytokines in secretions from allergic tissue, we suggest that IL-3-mediated inhibition of basophil apoptosis may exacerbate the inflammation associated with allergic disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Il-3 But Not Gm-csf þ Il-5 Inhibits Apoptosis In Human Matmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interleukin‐3, but not granulocyte–macrophage colony‐stimulating factor and interleukin‐5, inhibits apoptosis of human basophils through phosphatidylinositol 3‐kinase: requirement of NF‐κB‐dependent and ‐independent pathways

et al. 2002

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“…3). This concept of the term oncosis has found increased acceptance in recent studies (Park et al, 2000), and will also be used further in this paper.…”

Section: Morphologymentioning

confidence: 99%

Morphological and Biochemical Aspects of Apoptosis, Oncosis and Necrosis

Cruchten¹,

Broeck²

2002

Anat Histol Embryol

456

334

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Recent investigations have demonstrated the need for a precise differentiation of various forms of cell death such as apoptosis, oncosis, necrosis and programmed cell death. Apoptosis is marked by cellular shrinking, condensation and margination of the chromatin and ruffling of the plasma membrane with eventually breaking up of the cell in apoptotic bodies. Cell death marked by cellular swelling should be called oncosis, whereas the term necrosis refers to the morphological alterations appearing after cell death. Apoptosis and oncosis are therefore pre-mortal processes, while necrosis is a post-mortal condition. The term programmed cell death refers to the 'fixed' pathway followed by dying cells, whether or not with the characteristic morphology of apoptosis. Three mechanisms are actually known to be involved in the apoptotic process: a receptor-ligand mediated mechanism, a mitochondrial pathway and a mechanism in which the endoplasmic reticulum plays a central role. All three mechanisms activate caspases which are responsible for the characteristic morphological changes observed during apoptosis. A review of the different methods used for detecting apoptotic cells demonstrates that most of these techniques are not entirely specific.

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“…4b). Necrosis refers to cellular features after a cell has died (Park et al, 2000;Van Cruchten and Van Den Broeck, 2002). Oncosis as defined by Majno and Joris (1995) is a subdivision or special type of necrosis with specific cellular features such as cellular and organellar swelling, membrane disruption and changes in membrane permeability as well as absence of apoptotic bodies.…”

Section: Discussionmentioning

confidence: 99%

Effects of Urginea sanguinea, a traditional asthma remedy, on embryo neuronal development

Marx

Pretorius

Bester

2006

Journal of Ethnopharmacology

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Murine Bone Marrow-Derived Mast Cells Exhibit Evidence of Both Apoptosis and Oncosis After IL-3 Deprivation

Cited by 10 publications

References 23 publications

Interleukin‐3, but not granulocyte–macrophage colony‐stimulating factor and interleukin‐5, inhibits apoptosis of human basophils through phosphatidylinositol 3‐kinase: requirement of NF‐κB‐dependent and ‐independent pathways

Interleukin‐3, but not granulocyte–macrophage colony‐stimulating factor and interleukin‐5, inhibits apoptosis of human basophils through phosphatidylinositol 3‐kinase: requirement of NF‐κB‐dependent and ‐independent pathways

Morphological and Biochemical Aspects of Apoptosis, Oncosis and Necrosis

Effects of Urginea sanguinea, a traditional asthma remedy, on embryo neuronal development

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