2014Xiandai shengwu yixue jinzhanRequires access

Effects of the Different Degree of the Endoplasmic Reticulum Stress on Macrophage's Autophagy

MA Mei-jua

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Abstract

Objective: By using ox-LDL-induced macrophage foam cell model, we used different doses of tunicamycin to induce different degree of the endoplasmic reticulum stress, to observe the effects of it on autophagy. Methods: Different doses of tunicamycin were added to macrophage RAW264.7. The apoptosis rate was detected with TUNEL method. And the expression level of the endoplasmic reticulum stress marker protein GRP78 and autophagy marker protein P62 were detected by western blotting. Results: Compared with the ox-LDL group and the high-dose tunicamycin group, low-dose of tunicamycin significantly reduced the apoptosis of macrophage(P0.01); compared with ox-LDL group, the endoplasmic reticulum stress marker protein GRP78 expression was remarkable increased in low-dose tunicamycin group; meanwhile, the autophagy marker protein P62 moderately decreased(P0.01); in the high-dose tunicamycin group, there was more significant increase in the endoplasmic reticulum stress marker protein GRP78 expression, however the autophagy marker protein P62 also increased notably(P0.01). Conclusion: Low-dose of tunicamycin caused a certain degree of endoplasmic reticulum stress, which activated moderate autophagy, decreasing macrophage apoptosis. It may help to reduce the extent of the atherosclerosis.

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Objective: By using ox-LDL-induced macrophage foam cell model, we used different doses of tunicamycin to induce different degree of the endoplasmic reticulum stress, to observe the effects of it on autophagy. Methods: Different doses of tunicamycin were added to macrophage RAW264.7. The apoptosis rate was detected with TUNEL method. And the expression level of the endoplasmic reticulum stress marker protein GRP78 and autophagy marker protein P62 were detected by western blotting. Results: Compared with the ox-LDL group and the high-dose tunicamycin group, low-dose of tunicamycin significantly reduced the apoptosis of macrophage(P0.01); compared with ox-LDL group, the endoplasmic reticulum stress marker protein GRP78 expression was remarkable increased in low-dose tunicamycin group; meanwhile, the autophagy marker protein P62 moderately decreased(P0.01); in the high-dose tunicamycin group, there was more significant increase in the endoplasmic reticulum stress marker protein GRP78 expression, however the autophagy marker protein P62 also increased notably(P0.01). Conclusion: Low-dose of tunicamycin caused a certain degree of endoplasmic reticulum stress, which activated moderate autophagy, decreasing macrophage apoptosis. It may help to reduce the extent of the atherosclerosis.

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Available abstract

Objective: By using ox-LDL-induced macrophage foam cell model, we used different doses of tunicamycin to induce different degree of the endoplasmic reticulum stress, to observe the effects of it on autophagy. Methods: Different doses of tunicamycin were added to macrophage RAW264.7. The apoptosis rate was detected with TUNEL method. And the expression level of the endoplasmic reticulum stress marker protein GRP78 and autophagy marker protein P62 were detected by western blotting. Results: Compared with the ox-LDL group and the high-dose tunicamycin group, low-dose of tunicamycin significantly reduced the apoptosis of macrophage(P0.01); compared with ox-LDL group, the endoplasmic reticulum stress marker protein GRP78 expression was remarkable increased in low-dose tunicamycin group; meanwhile, the autophagy marker protein P62 moderately decreased(P0.01); in the high-dose tunicamycin group, there was more significant increase in the endoplasmic reticulum stress marker protein GRP78 expression, however the autophagy marker protein P62 also increased notably(P0.01). Conclusion: Low-dose of tunicamycin caused a certain degree of endoplasmic reticulum stress, which activated moderate autophagy, decreasing macrophage apoptosis. It may help to reduce the extent of the atherosclerosis.

Key concepts: Tunicamycin, Endoplasmic reticulum, Unfolded protein response, Autophagy, Apoptosis, Macrophage, Cell biology, Glucose-regulated protein

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