The Mechanism of Heat Shock Activation of ERK Mitogen-activated Protein Kinases in the Interleukin 3-dependent ProB Cell Line BaF3

Ng, Dominic C. H.; Bogoyevitch, Marie A.

doi:10.1074/jbc.m004639200

Cited by 41 publications

(20 citation statements)

References 61 publications

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“…However, its role in apoptosis remains controversial, with several studies suggesting that it may play either a proapoptotic [44][45][46] or an antiapoptotic [47,48] role in this process. Available evidence also suggests that heat stress can activate MAPK1/3 [49,50]. In the later study [50], we demonstrated the activation of MAPK1/3 in monkey Sertoli cells after testicular hyperthermia.…”

Section: Discussionmentioning

confidence: 74%

Mitogen-Activated Protein Kinase Signaling in Male Germ Cell Apoptosis in the Rat1

Jia

Castellanos

Wang

et al. 2009

Biology of Reproduction

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Programmed germ cell death is critical for functional spermatogenesis. Increased germ cell apoptosis can be triggered by various regulatory stimuli, including testicular hyperthermia or deprivation of gonadotropins and intratesticular testosterone. We have previously shown the involvement of the mitogen-activated protein kinase (MAPK) 14 in apoptotic signaling of male germ cells across species after hormone deprivation. This study investigates the role of MAPK14 in germ cell apoptosis in rats triggered by testicular hyperthermia. The contributions of the MAPK1/3 and the MAPK8 to male germ cell death were also examined after this intervention. We show that 1) testicular hyperthermia results in induction of both MAPK1/3 and MAPK14 but not MAPK8; 2) inhibition of MAPK1/3 has no effect on the incidence of heat-induced germ cell apoptosis, suggesting that MAPK1/3 signaling may be dispensable for heat-induced male germ cell apoptosis; and 3) activation of MAPK14 and BCL2 phosphorylation are critical for heat-induced male germ cell apoptosis in rats. Thus, unlike the hormone deprivation model, heat stress through activation of the MAPK14 signaling promotes germ cell apoptosis by provoking BCL2 phosphorylation, leading to its inactivation and the subsequent activation of the mitochondria-dependent death pathway. These novel findings point to a critical role of MAPK14 in stage- and cell-specific activation of male germ cell apoptosis triggered by hormone deprivation or heat stress.

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Section: Discussionmentioning

confidence: 74%

Mitogen-Activated Protein Kinase Signaling in Male Germ Cell Apoptosis in the Rat1

Jia

Castellanos

Wang

et al. 2009

Biology of Reproduction

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“…Preparation of Cellular Lysates-Cells (2 ϫ 10 7 ) were washed in cold phosphate-buffered saline and resuspended in lysis buffer (20 mM HEPES, pH 7.7, 2.5 mM MgCl 2 , 0.1 mM EDTA, 100 mM NaCl, 20 mM ␤-glycerophosphate, 20 g/ml leupeptin, 20 g/ml aprotinin, 100 g/ml phenylmethylsulfonyl fluoride, 100 M sodium orthovanadate, 500 M dithiothreitol, 1% (v/v) Nonidet P-40, 0.05% (v/v) Triton X-100) (26). Insoluble material was removed by centrifugation (20,800 ϫ g, 10 min, 4°C), the supernatants retained as the cellular lysates, and protein concentrations assayed (27).…”

Section: Gcsf-r Mutagenesis and Generation Of Stable Baf3mentioning

confidence: 99%

“…For assessment of JNK and ERK activity in the presence of the JNK inhibitor, Tat-TIJIP, lysate (200 g) from G-CSF-stimulated WT GCSF-R BaF3 cells was incubated with 40 g of GST-c-Jun or GST-Elk (26), complexes captured on glutathione-Sepharose 4B and divided into two aliquots. Samples were then treated with buffer or Tat-TIJIP (2 M) for 10 min at 30°C, prior to assaying of kinase activity by incubation with [␥-32 P]ATP as described above.…”

Section: Gcsf-r Mutagenesis and Generation Of Stable Baf3mentioning

confidence: 99%

Contribution of the Membrane-distal Tyrosine in Intracellular Signaling by the Granulocyte Colony-stimulating Factor Receptor

Kendrick

Lipscombe

Rausch

et al. 2004

Journal of Biological Chemistry

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We have evaluated the contribution of intracellular tyrosine residues of the granulocyte colony-stimulating factor receptor (GCSF-R) to its signaling and cellular outcomes. We began with stable BaF3 cell lines overexpressing wild-type or mutant GCSF-Rs. When all four intracellular tyrosines of the GCSF-R were replaced with phenylalanine (FFFF GCSF-R), cell proliferation and survival were compromised. Replacement of only the membrane-distal tyrosine (YYYF GCSF-R) also showed reduced survival following a GCSF withdrawal/ replacement protocol, suggesting a role for this tyrosine. Proliferation by FFFY GCSF-R cells was attenuated by ϳ70%. In evaluating the biochemical steps involved in signaling, we then showed that the membrane-distal tyrosine was necessary and sufficient for c-Jun N-terminal kinase (JNK) activation. With the use of a cell-permeable JNK-inhibitory peptide, JNK was implicated in the proliferation of the FFFY GCSF-R mutant. To further define the events linking the membranedistal tyrosine and JNK activation, the Src homology 2 domains of Shc, Grb2, and 3BP2 were shown to bind the full-length GCSF-R and a phosphopeptide encompassing the membrane-distal tyrosine. When binding to variant phosphopeptides based on this membrane-distal tyrosine was tested, altering the amino acids immediately following the phosphotyrosine could selectively abolish the interaction with Shc or Grb2, or the binding to both Grb2 and 3BP2. When these changes were introduced into the full-length GCSF-R and new cell lines created, only the mutant that did not interact with Grb2 and 3BP2 did not activate JNK. Our results suggest that direct binding of Shc by the GCSF-R is not essential for JNK activation.

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“…Moreover, the induction of AP-1 activity by asbestos was thought to be mediated through the activation of MAPK family, ERK1 and ERK2. The activation of ERK by proinflammatory stimuli was also thought to play important roles in innate immune responses and autoimmunity (Ng and Bogoyevitch 2000;Shaul and Seger 2007).…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression by chrysotile in human bronchial epithelial cells

Seo

Lee

2012

Animal Cells and Systems

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Asbestos exposure has been known to contribute to several lung diseases named asbestosis, malignant mesothelioma and lung cancer, but the disease-related molecular and cellular mechanisms are still largely unknown. To examine the effects of asbestos exposure in human bronchial epithelial cells at gene level, the global gene expression profile was analyzed following chrysotile treatment. The microarray results revealed differential gene expression in response to chrysotile treatment. The genes up-and down-regulated by chrysotile were mainly involved in processes including metabolism, signal transduction, transport, development, transcription, immune response, and other functions. The differential gene expression profiles could provide clues that might be used to understand the pathological mechanisms and therapeutic targets involved in chrysotile-related diseases.

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The Mechanism of Heat Shock Activation of ERK Mitogen-activated Protein Kinases in the Interleukin 3-dependent ProB Cell Line BaF3

Cited by 41 publications

References 61 publications

Mitogen-Activated Protein Kinase Signaling in Male Germ Cell Apoptosis in the Rat1

Mitogen-Activated Protein Kinase Signaling in Male Germ Cell Apoptosis in the Rat1

Contribution of the Membrane-distal Tyrosine in Intracellular Signaling by the Granulocyte Colony-stimulating Factor Receptor

Differential gene expression by chrysotile in human bronchial epithelial cells

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