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Activated protein C induces endoplasmic reticulum stress and attenuates lipopolysaccharide-induced apoptosis mediated by glycogen synthase kinase-3β.

Luo L, Lv T, Wang Q, Zhang T, Gu X, Xu F, Song Y - Mediators Inflamm. (2012)

Bottom Line: Calcium inhibition did not alter the antiapoptotic effect of activated protein C.The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA.In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.

ABSTRACT
This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.

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Calcium inhibition did not alter the antiapoptotic effect of APC. After exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h in the presence or absence of 50 μM TMB-8, an inhibitor of calcium release from the ER. There was no significant difference in the percentage of apoptosis cells between the two groups, which was detected by flow cytometric analysis (APC versus APC + TMB-8, P > 0.05).
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fig3: Calcium inhibition did not alter the antiapoptotic effect of APC. After exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h in the presence or absence of 50 μM TMB-8, an inhibitor of calcium release from the ER. There was no significant difference in the percentage of apoptosis cells between the two groups, which was detected by flow cytometric analysis (APC versus APC + TMB-8, P > 0.05).

Mentions: The inhibitor of calcium release, TMB-8, was used to investigate the influence of the transient rise of intracellular calcium-induced by APC on HUVEC apoptosis. The effective TMB-8 dose for inhibition of calcium release from the ER has been verified to be 50 μM. Therefore LPS-pretreated HUVECs were exposed to 150 nM APC in the presence or absence of TMB-8 (50 μM) for 0, 6, 12, and 24 h. Apoptosis of HUVECs were examined by flow cytometric analysis. No significant changes in apoptosis was observed in LPS-pretreated HUVECs between the two groups (APC versus APC + TMB-8, P > 0.05) (Figure 3).


Activated protein C induces endoplasmic reticulum stress and attenuates lipopolysaccharide-induced apoptosis mediated by glycogen synthase kinase-3β.

Luo L, Lv T, Wang Q, Zhang T, Gu X, Xu F, Song Y - Mediators Inflamm. (2012)

Calcium inhibition did not alter the antiapoptotic effect of APC. After exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h in the presence or absence of 50 μM TMB-8, an inhibitor of calcium release from the ER. There was no significant difference in the percentage of apoptosis cells between the two groups, which was detected by flow cytometric analysis (APC versus APC + TMB-8, P > 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368528&req=5

fig3: Calcium inhibition did not alter the antiapoptotic effect of APC. After exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h in the presence or absence of 50 μM TMB-8, an inhibitor of calcium release from the ER. There was no significant difference in the percentage of apoptosis cells between the two groups, which was detected by flow cytometric analysis (APC versus APC + TMB-8, P > 0.05).
Mentions: The inhibitor of calcium release, TMB-8, was used to investigate the influence of the transient rise of intracellular calcium-induced by APC on HUVEC apoptosis. The effective TMB-8 dose for inhibition of calcium release from the ER has been verified to be 50 μM. Therefore LPS-pretreated HUVECs were exposed to 150 nM APC in the presence or absence of TMB-8 (50 μM) for 0, 6, 12, and 24 h. Apoptosis of HUVECs were examined by flow cytometric analysis. No significant changes in apoptosis was observed in LPS-pretreated HUVECs between the two groups (APC versus APC + TMB-8, P > 0.05) (Figure 3).

Bottom Line: Calcium inhibition did not alter the antiapoptotic effect of activated protein C.The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA.In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.

ABSTRACT
This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.

Show MeSH
Related in: MedlinePlus