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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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APC attenuated LPS-induced apoptosis in HUVECs. Flow cytometric analysis of cultured HUVECs continuously exposed to 10 ng/mL LPS for 24 h revealed a high percentage of apoptotic cells (a). Subsequently, LPS-stimulated HUVECs were treated with 150 nM APC for 0, 6, 12 and 24 h ((a), (b), (c), and (d)). APC inhibition of cell apoptosis was detected following 6 h exposure ((b), (e); P < 0.05) and then generally decreased. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that 150 nM APC treatment markedly attenuated LPS-induced apoptosis in HUVECs.
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fig1: APC attenuated LPS-induced apoptosis in HUVECs. Flow cytometric analysis of cultured HUVECs continuously exposed to 10 ng/mL LPS for 24 h revealed a high percentage of apoptotic cells (a). Subsequently, LPS-stimulated HUVECs were treated with 150 nM APC for 0, 6, 12 and 24 h ((a), (b), (c), and (d)). APC inhibition of cell apoptosis was detected following 6 h exposure ((b), (e); P < 0.05) and then generally decreased. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that 150 nM APC treatment markedly attenuated LPS-induced apoptosis in HUVECs.

Mentions: As an initial step to clarify the antiapoptotic mechanism of APC, the effect of APC treatment on HUVECs survival following LPS stimulation was examined. Cells were continuously exposed to 10 ng/mL LPS for 24 h and subsequently treated with 150 nM APC for 0, 6, 12 and 24 h. It was observed that APC inhibited cell apoptosis markedly after 6 h of APC treatment. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that APC treatment markedly decreased the number of apoptotic cells (P < 0.05). Collectively, these data show that 150 nM APC treatment attenuated LPS-induced apoptosis in HUVECs (Figure 1).


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)

APC attenuated LPS-induced apoptosis in HUVECs. Flow cytometric analysis of cultured HUVECs continuously exposed to 10 ng/mL LPS for 24 h revealed a high percentage of apoptotic cells (a). Subsequently, LPS-stimulated HUVECs were treated with 150 nM APC for 0, 6, 12 and 24 h ((a), (b), (c), and (d)). APC inhibition of cell apoptosis was detected following 6 h exposure ((b), (e); P < 0.05) and then generally decreased. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that 150 nM APC treatment markedly attenuated LPS-induced apoptosis in HUVECs.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: APC attenuated LPS-induced apoptosis in HUVECs. Flow cytometric analysis of cultured HUVECs continuously exposed to 10 ng/mL LPS for 24 h revealed a high percentage of apoptotic cells (a). Subsequently, LPS-stimulated HUVECs were treated with 150 nM APC for 0, 6, 12 and 24 h ((a), (b), (c), and (d)). APC inhibition of cell apoptosis was detected following 6 h exposure ((b), (e); P < 0.05) and then generally decreased. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that 150 nM APC treatment markedly attenuated LPS-induced apoptosis in HUVECs.
Mentions: As an initial step to clarify the antiapoptotic mechanism of APC, the effect of APC treatment on HUVECs survival following LPS stimulation was examined. Cells were continuously exposed to 10 ng/mL LPS for 24 h and subsequently treated with 150 nM APC for 0, 6, 12 and 24 h. It was observed that APC inhibited cell apoptosis markedly after 6 h of APC treatment. Flow cytometric analysis of PI-Annexin V-FITC staining revealed that APC treatment markedly decreased the number of apoptotic cells (P < 0.05). Collectively, these data show that 150 nM APC treatment attenuated LPS-induced apoptosis in HUVECs (Figure 1).

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