Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes

Liu, Qinghang; Hofmann, Polly A.

doi:10.1152/ajpheart.01050.2003

Cited by 147 publications

(141 citation statements)

References 42 publications

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“…11,[27][28][29][30][31][32] We observed a strong significant positive association between the activation status of cytoplasmic JNK, p38, and ERK1/2 in superficial spreading melanomas as well as an association between activation of Akt and p38 in the cytoplasm. In a study by Pedram et al 32 expression of vascular endothelial growth factor was shown to induce a positive ERK1/2-JNK crosstalk in endothelial cells.…”

Section: Discussionmentioning

confidence: 97%

“…Moreover, our data are not in agreement with studies showing a negative cross-talk mechanism between p38 and ERK1/2 in several tissues. 11,[27][28][29] Common for these studies is the observation that inhibiting one pathway induces a robust increase in activation of the other and vice versa. This again demonstrates the complexity of signaling in different environments.…”

Section: Discussionmentioning

confidence: 99%

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Activation of c-jun N-terminal kinase is associated with cell proliferation and shorter relapse-free period in superficial spreading malignant melanoma

2006

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Signaling pathways regulating cell proliferation and survival have become attractive targets for anticancer strategies. In the present study, we analyzed by immunohistochemistry, a panel of benign nevi, superficial spreading and nodular primary melanomas and metastases for expression of activated p38/mitogen-activated protein kinase (p-p38) and c-jun N-terminal kinase (JNK) (p-JNK) and correlated the findings with known prognostic variables. Twenty-five and 35% of the primaries and 9 and 25% of the metastases expressed variable levels of p-p38 and p-JNK, respectively. In benign nevi, 73.5% expressed p-JNK and 7% expressed p-p38. For patients with superficial spreading melanomas, high level of cytoplasmic p-JNK was associated with thicker tumors (P ¼ 0.017) and shorter disease-free survival (P ¼ 0.003) as well as with markers of cell proliferation (cyclin A (P ¼ 0.017) and p21 (P ¼ 0.021)). In nodular melanomas, nuclear p-p38 was associated with Ki-67 (P ¼ 0.012), but neither cytoplasmic nor nuclear localized p-p38 was associated with disease outcome. Of note, in superficial spreading melanomas, a positive correlation between cytoplasmic p-JNK and cytoplasmic p-extracellular signal-regulated kinase ERK1/2 (P ¼ 0.005) and p-p38 (P ¼ 0.003) was observed. Likewise, p-p38 in cytoplasm was positively associated with cytoplasmic p-ERK1/2 (Po0.0005) and p-Akt (P ¼ 0.047). In contrast, except for a positive correlation between nuclear p-p38 and membranous p-TrkA (P ¼ 0.02), no correlation between the activation status of the different signaling pathways was observed in nodular melanomas. In conclusion, our results suggest that in benign nevi activated JNK may have a role in restricting uncontrolled cell proliferation or survival. However, during tumor progression, activation of JNK is associated with cell proliferation and shorter relapse-free period for patients with superficial spreading melanomas, suggesting that the JNK activation status could be a marker for clinical outcome in at least a subgroup of malignant melanoma. In contrast, activation of p38 seems to play a less important role in development and progression of malignant melanomas.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Activation of c-jun N-terminal kinase is associated with cell proliferation and shorter relapse-free period in superficial spreading malignant melanoma

2006

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“…Syntaxin 1A has been shown to be phosphorylated by different protein kinases, and phosphorylation of syntaxin 1A regulates its interaction with other proteins (Foletti et al, 2000;Tian et al, 2003). p38 MAPK regulates the activity and translocation of PP2Ac (Liu and Hofmann, 2004). Thus, phosphatase activity from the SERT-P2Ac complex may participate at different levels, maintaining appropriate levels of functional SERTs to coordinate with various cellular stimuli.…”

Section: Discussionmentioning

confidence: 99%

A Role for p38 Mitogen-Activated Protein Kinase in the Regulation of the Serotonin Transporter: Evidence for Distinct Cellular Mechanisms Involved in Transporter Surface Expression

Samuvel¹,

Jayanthi²,

Bhat³

et al. 2005

J. Neurosci.

198

260

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“…62 Moreover, PP2A mediates a cross talk between p38 MAPK and ERK in cardiac myocytes, as shown by increased ERK phosphorylation in H 2 O 2 -stimulated ventricular myocytes in response to okadaic acid. 60 Based on these observations, it can be imagined that p38 MAPK might regulate HQ-induced ERK activation through PP2A in ARPE-19 cells. Future studies will test this hypothesis.…”

Section: Hsp27 and Oxidative Stress In Rpe 1211mentioning

confidence: 99%

“…63 One-way cross talk between p38 and ERK has been reported in various cells. 60,64,65 To further investigate the relationship between p38 and ERK pathways in response to HQ in ARPE-19 cells, we examined the effects of MEK inhibitor PD98059 on HQ-induced phosphorylation of p38. We found that PD98059 decreased HQ-induced p38 MAPK activation indicating that ERK1/2 pathway positively modulates p38 signaling and that ERK is required for HQ-induced activation of p38 MAPK signaling pathway in human RPE cells.…”

Section: Hsp27 and Oxidative Stress In Rpe 1211mentioning

confidence: 99%

Cigarette Smoke-Related Hydroquinone Induces Filamentous Actin Reorganization and Heat Shock Protein 27 Phosphorylation through p38 and Extracellular Signal-Regulated Kinase 1/2 in Retinal Pigment Epithelium

Pons

Cousins

Csaky

et al. 2010

The American Journal of Pathology

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Retinal pigment epithelium (RPE)-derived membranous debris named blebs, may accumulate and contribute to sub-RPE deposit formation, which is the earliest sign of age-related macular degeneration (AMD). Oxidative injury to the RPE might play a significant role in AMD. However, the underlying mechanisms are unknown. We previously reported that hydroquinone (HQ), a major pro-oxidant in cigarette smoke, foodstuff, and atmospheric pollutants, induces actin rearrangement and membrane blebbing in RPE cells as well as sub-RPE deposits in mice. Here, we show for the first time that phosphorylated Heat shock protein 27 (Hsp27), a key regulator of actin filaments dynamics, is up-regulated in RPE from patients with AMD. Also, HQ-induced nonlethal oxidative injury led to Hsp27mRNA up-regulation, dimer formation , and Hsp27 phosphorylation in ARPE-19 cells. Furthermore, we found that a cross talk between p38 and extracellular signal-regulated kinase (ERK) mediates HQ-induced Hsp27 phosphorylation and actin aggregate formation, revealing ERK as a novel upstream mediator of Hsp27 phosphorylation. Finally, we demonstrated that Hsp25, p38, and ERK phosphorylation are increased in aging C57BL/6 mice chronically exposed to HQ, whereas Hsp25 expression is decreased. Our data suggest that phosphorylated Hsp27 might be a key mediator in AMD and HQ-induced oxidative injury to the RPE, which may provide helpful insights into the early cellular events associated with actin reorganization and bleb formation involved in sub-RPE deposits formation relevant to the pathogenesis of AMD.

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Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes

Cited by 147 publications

References 42 publications

Activation of c-jun N-terminal kinase is associated with cell proliferation and shorter relapse-free period in superficial spreading malignant melanoma

Activation of c-jun N-terminal kinase is associated with cell proliferation and shorter relapse-free period in superficial spreading malignant melanoma

A Role for p38 Mitogen-Activated Protein Kinase in the Regulation of the Serotonin Transporter: Evidence for Distinct Cellular Mechanisms Involved in Transporter Surface Expression

Cigarette Smoke-Related Hydroquinone Induces Filamentous Actin Reorganization and Heat Shock Protein 27 Phosphorylation through p38 and Extracellular Signal-Regulated Kinase 1/2 in Retinal Pigment Epithelium

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