Relationship between Apoptosis and the Cell Cycle in Lymphocytes: Roles of Protein Kinase C, Tyrosine Phosphorylation, and AP1

Pr, Walker; Kwast‐Welfeld, Joanna; Gourdeau, Henriette; Leblanc, Julie; Neugebauer, Witold; Sikorska, Marianna

doi:10.1006/excr.1993.1173

Cited by 112 publications

(55 citation statements)

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“…These results suggest that the IL-2 refractory phenotype of the previously undivided CD4 ϩ T cells is due to a biochemical defect that lies somewhere upstream of the action of PKC within the PI 3 K-PKB/Akt pathway. PKC is normally coupled to the IL-2R through PI 3 K, as PKC is activated by PDK1-dependent phosphorylation (40), and a role for PKC in IL-2-mediated signal transduction has been defined using the IL-2-dependent cell line CTLL (59,60). Interestingly, full activation of the PKC-␦ isoform requires the activity of mTOR/FRAP (61), which is in turn dependent on PKB/Akt (62).…”

Section: Discussionmentioning

confidence: 99%

T Cell Effector Function and Anergy Avoidance Are Quantitatively Linked to Cell Division

Wells

Walsh

Sankaran

et al. 2000

The Journal of Immunology

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We have shown previously that T cells activated by optimal TCR and CD28 ligation exhibit marked proliferative heterogeneity, and ∼40% of these activated cells fail entirely to participate in clonal expansion. To address how prior cell division influences the subsequent function of primary T cells at the single cell level, primary CD4+ T cells were subjected to polyclonal stimulation, sorted based on the number of cell divisions they had undergone, and restimulated by ligation of TCR/CD28. We find that individual CD4+ T cells exhibit distinct secondary response patterns that depend upon their prior division history, such that cells that undergo more rounds of division show incrementally greater IL-2 production and proliferation in response to restimulation. CD4+ T cells that fail to divide after activation exist in a profoundly hyporesponsive state that is refractory to both TCR/CD28-mediated and IL-2R-mediated proliferative signals. We find that this anergic state is associated with defects in both TCR-coupled activation of the p42/44 mitogen-activated protein kinase (extracellular signal-related kinase 1/2) and IL-2-mediated down-regulation of the cell cycle inhibitor p27kip1. However, these defects are selective, as TCR-mediated intracellular calcium flux and IL-2R-coupled STAT5 activation remain intact in these cells. Therefore, the process of cell division or cell cycle progression plays an integral role in anergy avoidance in primary T cells, and may represent a driving force in the formation of the effector/memory T cell pool.

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Section: Discussionmentioning

confidence: 99%

T Cell Effector Function and Anergy Avoidance Are Quantitatively Linked to Cell Division

Wells

Walsh

Sankaran

et al. 2000

The Journal of Immunology

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“…Flow cytometric analysis of the Bcap-37 cell cycle was performed according to the method described previously (Walker et al, 1993). The cells were collected by centrifugation at 1000 rpm on a TGL-80-2B centrifuge (ShangHai Anting Scientific Instrument Factory) for 5 min and thoroughly rinsed with PBS.…”

Section: Flow Cytometric Assay For Bcap-37 Cellsmentioning

confidence: 99%

Effect of themicrobial lipopeptide on tumor cell lines: apoptosis induced by disturbing the fatty acid composition of cell membrane

Tao

Zou

et al. 2010

Protein Cell

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Microbial lipopeptides play an important role in apoptosis induction of tumor cells. However, there is little knowledge about the relationship between apoptosis induction and membrane fatty acids. The present study focused on the effects of lipopeptides produced by Bacillus subtilis HSO121 on Bcap-37 cell lines. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl (MTT) colorimetric assay and surface tension measurements, showed that the critical micelle concentration (CMC) was a critical level for the inhibitory activity of lipopeptides on the growth of Bcap-37 cells. Under the CMC, the order of least to greatest cytotoxicity effect on cancer cell lines by lipopeptides is C 13 -lipopeptide < C 14 -lipopepitde < C 15 -lipopeptide. Above CMC, all lipopeptides directly exert cytolytic activity. The flow cytometric analysis and Hoechst33258 staining experiments confirmed the apoptosis of Bcap-37 cell lines induced by lipopeptides in a dose-dependent manner. This apoptosis was associated with a significant decrease of the unsaturated degree of the cellular fatty acids of Bcap-37 cell lines due to the changes in the cellular fatty acids composition induced by the lipopeptide treatment. These results indicated that disturbance of the cellular fatty acid composition of breast cancer cell lines were related to in the cell apoptosis. Furthermore, significant difference in IC 50 values of tumor cells and normal cell showed that the lipopeptide exerted selective cytotoxicity on the cancer cells. Thus HSO121 lipopeptides may have potential applications as an anticancer leads.

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“…2 This interpretation is consistent with earlier findings indicating that in cytokine (IL-2)-dependent CTLL cells there is a correlation between the presence of AP-1 DNA binding activity and repression of corticosteroid-induced apoptosis. 5 In the absence of interleukin-2, corticosteroid treatment stimulates AP-1 degradation and induces apoptosis. 5 The repression of AP-1 transcription factor activity in corticosteroid-treated lymphocytes is accompanied by repression of other prosurvival transcription factors, including the nuclear factor of activated T lymphocytes (NFAT).…”

Section: Evidence For Involvement Of the Glucocorticoid Receptor Tranmentioning

confidence: 99%

“…5 In the absence of interleukin-2, corticosteroid treatment stimulates AP-1 degradation and induces apoptosis. 5 The repression of AP-1 transcription factor activity in corticosteroid-treated lymphocytes is accompanied by repression of other prosurvival transcription factors, including the nuclear factor of activated T lymphocytes (NFAT). 6 NFAT is composed of two components, NFATp and AP-1; the dexamethasone-induced decrease in NFAT activity is due to a decrease in AP-1 activity.…”

Section: Evidence For Involvement Of the Glucocorticoid Receptor Tranmentioning

confidence: 99%

Recent insights into the mechanism of glucocorticosteroid-induced apoptosis

2002

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Glucocorticosteroid hormones induce apoptosis in lymphocytes. Therefore, glucocorticoids are commonly used as immunosuppressive and chemotherapeutic agents. This review examines many facets of the process by which glucocorticoids induce apoptosis. This process is divided into three stages, an initiation stage that involves glucocorticoid receptor-mediated gene regulation, a decision stage that involves the counterbalancing influence of prosurvival and proapoptotic factors, and the execution stage which involves caspase and endonuclease activation. Many aspects of glucocorticoid-induced apoptosis, such as mitochondrial dysfunction and caspase activation, are important steps in virtually all forms of apoptosis. But the process glucocorticoid-induced apoptosis differs from other forms of apoptosis in terms of initiation at the transcriptional level and involvement of the multicatalytic proteasome and calcium. Moreover, the abundant opportunity for crosstalk between the glucocorticoid receptor and other signaling pathways increases the complexity of glucocorticoid-induced apoptosis and its regulation.

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Relationship between Apoptosis and the Cell Cycle in Lymphocytes: Roles of Protein Kinase C, Tyrosine Phosphorylation, and AP1

Cited by 112 publications

References 0 publications

T Cell Effector Function and Anergy Avoidance Are Quantitatively Linked to Cell Division

T Cell Effector Function and Anergy Avoidance Are Quantitatively Linked to Cell Division

Effect of themicrobial lipopeptide on tumor cell lines: apoptosis induced by disturbing the fatty acid composition of cell membrane

Recent insights into the mechanism of glucocorticosteroid-induced apoptosis

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