Participation of various kinases in staurosporine-induced apoptosis of RAW 264.7 cells

Yamaki, Kouya; Hong, Jin-Kyung; Hiraizumi, Kenji; Ahn, Jae Pyung; Zee, Ok-Pyo; Ohuchi, Kazuo

doi:10.1211/002235702144

Cited by 26 publications

(22 citation statements)

References 43 publications

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“…For example, ERK has been reported to be an important macrophage survival factor in some (35)(36)(37)(38)(39)(40) but not all (30,41,42) studies, and we detected decreased ERK phosphorylation in response to LPS or thapsigargin in BMDMs from both WT and BCAP-deficient mice, as well as a trend for enhanced ERK phosphorylation in unchallenged BMDMs from BCAP-deficient mice (Fig. 4).…”

Section: Bcap Is Required For Maximal Activation Of Akt In Response Tsupporting

confidence: 53%

A Requirement for the p85 PI3K Adapter Protein BCAP in the Protection of Macrophages from Apoptosis Induced by Endoplasmic Reticulum Stress

Song

Chew

Dale

et al. 2011

The Journal of Immunology

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Macrophages are innate immune cells that play key roles in regulation of the immune response and in tissue injury and repair. In response to specific innate immune stimuli, macrophages may exhibit signs of endoplasmic reticulum (ER) stress and progress to apoptosis. Factors that regulate macrophage survival under these conditions are poorly understood. In this study, we identified B cell adapter protein (BCAP), a p85 PI3K-binding adapter protein, in promoting survival in response to the combined challenge of LPS and ER stress. BCAP was unique among nine PI3K adapter proteins in being induced >10-fold in response to LPS. LPS-stimulated macrophages incubated with thapsigargin, a sarcoplasmic/endoplasmic reticulum calcium ATPase inhibitor that induces ER stress, underwent caspase-3 activation and apoptosis. Macrophages from BCAP−/− mice exhibited increased apoptosis in response to these stimuli. BCAP-deficient macrophages demonstrated decreased activation of Akt, but not ERK, and, unlike BCAP-deficient B cells, expressed normal amounts of the NF-κB subunits, c-Rel and RelA. Retroviral transduction of BCAP-deficient macrophages with wild-type BCAP, but not a Y4F BCAP mutant defective in binding the SH2 domain of p85 PI3K, reversed the proapoptotic phenotype observed in BCAP-deficient macrophages. We conclude that BCAP is a nonredundant PI3K adapter protein in macrophages that is required for maximal cell survival in response to ER stress. We suggest that as macrophages engage their pathogenic targets, innate immune receptors trigger increased expression of BCAP, which endows them with the capacity to withstand further challenges from ongoing cellular insults, such as ER stress.

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Section: Bcap Is Required For Maximal Activation Of Akt In Response Tsupporting

confidence: 53%

A Requirement for the p85 PI3K Adapter Protein BCAP in the Protection of Macrophages from Apoptosis Induced by Endoplasmic Reticulum Stress

Song

Chew

Dale

et al. 2011

The Journal of Immunology

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“…ST can inhibit many different protein kinases involved in diverse aspects of cellular metabolism (Yamaki et al, 2002). It is striking that this broad-spectrum kinase inhibitor specifically rescued the biological process of root hair growth in both PIDox and PIN3ox roots ( Figures 4E, 5, 8G, and 8H).…”

Section: Discussion the Root Hair System As A Model For Auxin Transportmentioning

confidence: 94%

PINOID Positively Regulates Auxin Efflux inArabidopsisRoot Hair Cells and Tobacco Cells

2006

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Intercellular transport of auxin is mediated by influx and efflux carriers in the plasma membrane and subjected to developmental and environmental regulation. Here, using the auxin-sensitive Arabidopsis thaliana root hair cell system and the tobacco (Nicotiana tabacum) suspension cell system, we demonstrate that the protein kinase PINOID (PID) positively regulates auxin efflux. Overexpression of PID (PIDox) or the auxin efflux carrier component PINFORMED3 (PIN3, PIN3ox), specifically in the root hair cell, greatly suppressed root hair growth. In both PIDox and PIN3ox transformants, root hair growth was nearly restored to wild-type levels by the addition of auxin, protein kinase inhibitors, or auxin efflux inhibitors. Localization of PID or PIN3 at the cell boundary was disrupted by brefeldin A and staurosporine. A mutation in the kinase domain abrogated the ability of PID to localize at the cell boundary and to inhibit root hair growth. These results suggest that PIDox-or PIN3ox-enhanced auxin efflux results in a shortage of intracellular auxin and a subsequent inhibition of root hair growth. In an auxin efflux assay using transgenic tobacco suspension cells, PIDox or PIN3ox also enhanced auxin efflux. Collectively, these results suggest that PID positively regulates cellular auxin efflux, most likely by modulating the trafficking of PIN and/or some other molecular partners involved in auxin efflux.

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“…3). Both agents induce apoptosis by way of several pro-apoptotic mechanisms (25)(26)(27). Thus, it is likely that an alteration of more than one signaling pathway, involving cascades for apoptosis or survival, is responsible for reduced PICD in CBMO.…”

Section: Discussionmentioning

confidence: 99%

Diminished Phagocytosis-Induced Cell Death (PICD) in Neonatal Monocytes upon Infection with Escherichia coli

et al. 2008

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An imbalance in apoptosis or survival of immune cells plays an essential role in the pathophysiology of sepsis. Phagocytosis-induced cell death (PICD) is a common result of the pathogenhost cell interaction mediated by reactive oxygen species (ROS). Neonatal sepsis is frequently characterized by hyperinflammation. Cord blood monocytes (CBMO) are equivalent to monocytes of adults [peripheral blood monocytes (PBMO)], both in terms of phagocytosis and killing of Escherichia coli. We investigated whether CBMO are less sensitive toward PICD compared with PBMO. Monocytes were infected with green fluorescent protein (GFP)-labeled E. coli. Phagocytic activity, cell-count, Annexin V staining, hypoploid DNA content, CD95 and CD95L expression, and caspase-8 and -9 activities were analyzed by flow cytometry, ROS production by chemiluminescence, and CD95L mRNA expression by reverse-transcriptase polymerase chain reaction. With equal phagocytic activity and ROS production, PBMO cell count was decreased by 82 Ϯ 6% versus 28 Ϯ 8% for CBMO after infection. Annexin V binding was enhanced fivefold on PBMO; 56 Ϯ 15% of PBMO showed a hypodiploid DNA content compared with 9 Ϯ 6% of CBMO. Caspases CD95L and CD95L mRNA were up-regulated in PBMO. Our results indicate that CBMO are less sensitive toward E. coli-mediated PICD than PBMO. Modifying monocyte apoptosis may be a target for future interventions in sepsis. (Pediatr Res 63: [33][34][35][36][37][38] 2008)

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Participation of various kinases in staurosporine-induced apoptosis of RAW 264.7 cells

Cited by 26 publications

References 43 publications

A Requirement for the p85 PI3K Adapter Protein BCAP in the Protection of Macrophages from Apoptosis Induced by Endoplasmic Reticulum Stress

A Requirement for the p85 PI3K Adapter Protein BCAP in the Protection of Macrophages from Apoptosis Induced by Endoplasmic Reticulum Stress

PINOID Positively Regulates Auxin Efflux inArabidopsisRoot Hair Cells and Tobacco Cells

Diminished Phagocytosis-Induced Cell Death (PICD) in Neonatal Monocytes upon Infection with Escherichia coli

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