Pervanadate elicits proliferation and mediates activation of mitogen‐activated protein (MAP) kinase in the nucleus<sup>1</sup>

Krady, Marie-Marthe; Freyermuth, Solange; Rogue, P; Malviya, Anant N.

doi:10.1016/s0014-5793(97)00821-1

Cited by 24 publications

(22 citation statements)

References 26 publications

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“…We found that lower micromolar concentrations of bpV (phen) stimulate RINm5F cell survival, which is in agreement with the studies in rat pheochromocytoma PC12 cells (Cerovac et al, 1999), endothelial cells (Natarajan et al, 2001) and C3H10T1/2 embryonic mouse ¢broblasts (Krady et al, 1997). We suggest that the mechanism underlying this survival-enhancing e¡ect could be associated with bpV (phen)-induced ERK activation and MKP-1 expression.…”

Section: Discussionsupporting

confidence: 90%

“…Furthermore, vanadate exhibits mitogenic properties in SV40-transformed cells (Wang and Scott, 1995). In C3H10T1/3 mouse ¢broblasts peroxovanadates formed in situ have been found to lead to proliferation (Krady et al, 1997). However, vanadium can also exhibit cytotoxic and antineoplastic e¡ects both in vivo and in vitro (Cruz et al, 1995;Morinville et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

et al. 2004

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Lower micromolar concentrations of peroxovanadium compound potassium bisperoxo(1,10-phenanthroline)oxovanadate (V) [bpV (phen)] stimulate RINm5F cell metabolic activity. 1 and 3 micromol/L bpV (phen) induces strong and sustained activation of extracellular signal-regulated kinase (ERK). However, it seems that bpV (phen) does not effect c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) phosphorylation. In addition, bpV (phen) induces mitogen-activated protein kinase phosphatase-1 (MKP-1) expression. We found that ERK activation could be completely abolished if RINm5F cells were incubated with both bpV (phen) and PD 98059, a specific inhibitor of upstream ERK kinase MEK1. On the other hand, this combined treatment up-regulated activation of stress kinases, JNK and p38 MAPK, significantly suppressed MKP-1 expression and induced cell death. Thus, our results suggest that the mechanism underlying bpV (phen) survival-enhancing effect could be associated with induced ERK activation and MKP-1 expression.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

et al. 2004

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“…Plasma was separated from packed cells and cell counting was done as described. 15 Cells were plated in 30-mm Petri dishes at a density of 1 . 25 Â 10 5 cells per dish and allowed to grow.…”

Section: Methodsmentioning

confidence: 99%

Erythrocyte lipid peroxidation and antioxidants in cigarette smokers

Codandabany

2000

Cell Biochem. Funct.

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The present study has analysed the relationship between lipid peroxidation and antioxidant status in erythrocytes from 30 adult male cigarette smokers and an equal number of age and sex-matched normal subjects. Erythrocyte lipid peroxidation was markedly increased. The enzymic antioxidants were decreased in erythrocytes of cigarette smokers. The present study highlights the occurrence of lipid peroxidation and possible breakdown of antioxidant status in cigarette smoking.

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“…It has been reported that TPA stimulated MAPK activity in C3H 10T1/2 cells (Krady et al, 1997), but the involvement of MAPK activation in TPA-stimulated cyclin D1 induction has not yet been established. In Figure 4a, the contribution of MEK/MAPK activation towards TPA-stimulated cyclin D1 induction was examined with application of PD98059.…”

Section: Tpa Induces Cyclin D1 and Activates Both Pkce And Pkcamentioning

confidence: 98%

Modulation of cyclin D1 and its signaling components by the phorbol ester TPA and the tyrosine phosphatase inhibitor vanadate

Song

Wenner

2001

J. Cell. Physiol.

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The mechanism by which 12-O-tetradecanoylphorbol-13-acetate (TPA) triggers cell-cycle progression at G1 phase in mouse embryonic fibroblast C3H 10T1/2 cells was examined. TPA treatment resulted in a temporary induction of cyclin D1 peaking at 9 h post stimulation. PD98059 (10 microM), the specific inhibitor of MAPK kinase, completely blocked TPA-stimulated cyclin D1 induction and DNA synthesis, confirming that MAPK activation plays an essential role in TPA-stimulated cell-cycle progression. Although both PKCalpha and PKCepsilon are expressed in C3H 10T1/2 cells, inhibitor studies suggest that PKCepsilon activation is required for the activation of MEK/MAPK signal transduction cascade. p70s6K, an important kinase involved in the regulation of protein synthesis and cell-cycle progression, has been reported to be activated through a PKC-dependent pathway (TPA-activatable) in addition to a PI3K-dependent pathway. Here, we demonstrate for the first time that TPA-stimulated MAPK activation is essential for the phosphorylation of several key residues involved in the activation of p70s6K, namely, thr389, thr421, and ser424. Vanadate, the tyrosine phosphatase inhibitor, triggered a sustained elevation of the level of active MAPK. However, corresponding to a rapid loss of cyclin D1 protein, vanadate treatment resulted in a significant shut out of 3H-thymidine incorporation into DNA regardless of TPA cotreatment. Vanadate treatment also led to the increase of active MEK, increased phosphorylation of p70s6K at thr389, thr421, and ser424 yet without activation of PKB. These data suggest that vanadate can selectively perturb the activation of signaling components which raises the interesting issue as to how vanadate downregulates the cyclin D1 level.

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Pervanadate elicits proliferation and mediates activation of mitogen‐activated protein (MAP) kinase in the nucleus¹

Cited by 24 publications

References 26 publications

Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

Erythrocyte lipid peroxidation and antioxidants in cigarette smokers

Modulation of cyclin D1 and its signaling components by the phorbol ester TPA and the tyrosine phosphatase inhibitor vanadate

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Pervanadate elicits proliferation and mediates activation of mitogen‐activated protein (MAP) kinase in the nucleus1

Cited by 24 publications

References 26 publications

Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

Positive regulation of ERK activation and MKP-1 expression by peroxovanadium complex bpV (phen)

Erythrocyte lipid peroxidation and antioxidants in cigarette smokers

Modulation of cyclin D1 and its signaling components by the phorbol ester TPA and the tyrosine phosphatase inhibitor vanadate

Contact Info

Product

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Pervanadate elicits proliferation and mediates activation of mitogen‐activated protein (MAP) kinase in the nucleus¹