Limits...
Verrucarin A Inhibition of MAP Kinase Activation in a PMA-stimulated Promyelocytic Leukemia Cell Line

View Article: PubMed Central

ABSTRACT

Verrucarin A is an inhibitor of protein synthesis. In this study, we examined the inhibitory action of verrucarin A on signal molecules. Verrucarin A partially inhibited the IL-8 production of a PMA-stimulated promyelocytic leukemia cell line (HL-60 cells), and the effect was related to the inhibition of NF-κB activation at non-cytotoxic concentrations. Moreover, the inhibition of mitogen activated protein (MAP) kinase by verrucarin A was especially strong with p38- and JNK-phosphorylation. The findings show a new action of verrucarin A, and it is expected that this action relaxes the signal activation in response to stress.

No MeSH data available.


Related in: MedlinePlus

Effects of verrucarin A, verrucarin J and roridin E on IL-8 production and cell proliferation in PMA-stimulated HL-60 cells. A), C) and E) show effects of verrucarin A, verrucarin J and roridin E, respectively, on IL-8 production. HL-60 cells (1 x 106 cells/ml) were treated with PMA (20 nM) and the indicated concentrations of the compounds for 24 h. The IL-8 concentration in the culture supernatant of the PMA-stimulated cells was determined to be ca. 24 ng/ml by ELISA as described in Materials and Methods. The data are shown as values relative (%) to the PMA-stimulated IL-8 production (24 ng/ml). The data are the mean values of three independent experiments. B), D) and F) show the effects of verrucarin A, verrucarin J and roridin E, respectively, on cell proliferation. The MTT assay was as described in Materials and Methods. The data are shown as values relative (%) to the value of PMA-stimulated condition. The data are the mean values of three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3756328&req=5

f2-marinedrugs-03-00064: Effects of verrucarin A, verrucarin J and roridin E on IL-8 production and cell proliferation in PMA-stimulated HL-60 cells. A), C) and E) show effects of verrucarin A, verrucarin J and roridin E, respectively, on IL-8 production. HL-60 cells (1 x 106 cells/ml) were treated with PMA (20 nM) and the indicated concentrations of the compounds for 24 h. The IL-8 concentration in the culture supernatant of the PMA-stimulated cells was determined to be ca. 24 ng/ml by ELISA as described in Materials and Methods. The data are shown as values relative (%) to the PMA-stimulated IL-8 production (24 ng/ml). The data are the mean values of three independent experiments. B), D) and F) show the effects of verrucarin A, verrucarin J and roridin E, respectively, on cell proliferation. The MTT assay was as described in Materials and Methods. The data are shown as values relative (%) to the value of PMA-stimulated condition. The data are the mean values of three independent experiments.

Mentions: Therefore, the effects of verrucarin A, verrucarin J and roridin E on IL-8 production by PMA-stimulated HL-60 cells were examined, and the results are shown in Figure 2A, C and E. Verrucarin A and roridin E inhibited IL-8 production by PMA-stimulated HL-60 cells, but the inhibition by roridin E and verrucarin A (0.1 and 1 μg/ml) correlated with cell proliferation in the MTT assay. Therefore, it is estimated that the inhibition by roridin E and verrucarin A (0.1 and 1 μg/ml) is due to their cytotoxicity. On the other hand, verrucarin A (1 and 10 ng/ml) did not affect cell proliferation. Therefore, verrucarin A was of interest.


Verrucarin A Inhibition of MAP Kinase Activation in a PMA-stimulated Promyelocytic Leukemia Cell Line
Effects of verrucarin A, verrucarin J and roridin E on IL-8 production and cell proliferation in PMA-stimulated HL-60 cells. A), C) and E) show effects of verrucarin A, verrucarin J and roridin E, respectively, on IL-8 production. HL-60 cells (1 x 106 cells/ml) were treated with PMA (20 nM) and the indicated concentrations of the compounds for 24 h. The IL-8 concentration in the culture supernatant of the PMA-stimulated cells was determined to be ca. 24 ng/ml by ELISA as described in Materials and Methods. The data are shown as values relative (%) to the PMA-stimulated IL-8 production (24 ng/ml). The data are the mean values of three independent experiments. B), D) and F) show the effects of verrucarin A, verrucarin J and roridin E, respectively, on cell proliferation. The MTT assay was as described in Materials and Methods. The data are shown as values relative (%) to the value of PMA-stimulated condition. The data are the mean values of three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3756328&req=5

f2-marinedrugs-03-00064: Effects of verrucarin A, verrucarin J and roridin E on IL-8 production and cell proliferation in PMA-stimulated HL-60 cells. A), C) and E) show effects of verrucarin A, verrucarin J and roridin E, respectively, on IL-8 production. HL-60 cells (1 x 106 cells/ml) were treated with PMA (20 nM) and the indicated concentrations of the compounds for 24 h. The IL-8 concentration in the culture supernatant of the PMA-stimulated cells was determined to be ca. 24 ng/ml by ELISA as described in Materials and Methods. The data are shown as values relative (%) to the PMA-stimulated IL-8 production (24 ng/ml). The data are the mean values of three independent experiments. B), D) and F) show the effects of verrucarin A, verrucarin J and roridin E, respectively, on cell proliferation. The MTT assay was as described in Materials and Methods. The data are shown as values relative (%) to the value of PMA-stimulated condition. The data are the mean values of three independent experiments.
Mentions: Therefore, the effects of verrucarin A, verrucarin J and roridin E on IL-8 production by PMA-stimulated HL-60 cells were examined, and the results are shown in Figure 2A, C and E. Verrucarin A and roridin E inhibited IL-8 production by PMA-stimulated HL-60 cells, but the inhibition by roridin E and verrucarin A (0.1 and 1 μg/ml) correlated with cell proliferation in the MTT assay. Therefore, it is estimated that the inhibition by roridin E and verrucarin A (0.1 and 1 μg/ml) is due to their cytotoxicity. On the other hand, verrucarin A (1 and 10 ng/ml) did not affect cell proliferation. Therefore, verrucarin A was of interest.

View Article: PubMed Central

ABSTRACT

Verrucarin A is an inhibitor of protein synthesis. In this study, we examined the inhibitory action of verrucarin A on signal molecules. Verrucarin A partially inhibited the IL-8 production of a PMA-stimulated promyelocytic leukemia cell line (HL-60 cells), and the effect was related to the inhibition of NF-κB activation at non-cytotoxic concentrations. Moreover, the inhibition of mitogen activated protein (MAP) kinase by verrucarin A was especially strong with p38- and JNK-phosphorylation. The findings show a new action of verrucarin A, and it is expected that this action relaxes the signal activation in response to stress.

No MeSH data available.


Related in: MedlinePlus