AACE ePoster Library

BETA BLOCKERS SUPPRESS DEXTROSE-INDUCED ENDOPLASMIC RETICULUM STRESS, OXIDATIVE STRESS AND APOPTOSIS IN HUMAN CORONARY ARTERY ENDOTHELIAL CELLS.
AACE ePoster Library. Shah H. 05/13/15; 97758; 402
Harshit Shah
Harshit Shah
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Abstract
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Background: Beta blockers are known to have favorable effects on endothelial function partly because of their capacity to reduce oxidative stress.
Methods and Results: To determine if beta blockers can also prevent dextrose-induced endoplasmic reticulum (ER) stress in addition to their anti-oxidative effects, human coronary artery endothelial cells and hepatocyte-derived HepG2 cells were treated with 27.5 mM dextrose for 24 hours in the presence of carvedilol (a lipophilic beta blockers with alpha blocking activity), propranolol (a lipophilic non selective beta blockers) and atenolol (a water-soluble selective beta blockers) and ER stress, oxidative stress and cell death were measured.
ER stress was measured using the placental alkaline phosphatase assay and western blot analysis of glucose regulated protein 78, c-jun-N-terminal kinase (JNK), phospho-JNK, eukaryotic initiating factor 2α (eIF2α) and phospho-eIF2α and measurement of X-box binding protein 1 (XBP1) mRNA splicing using reverse transcriptase-polymerase chain reaction. Superoxide (SO) generation was measured using the superoxide-reactive probe 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-A]pyrazin-3-one hydrochloride (MCLA) chemiluminescence. Cell viability was measured by propidium iodide (PI) staining method.
The ER stress, SO production and cell death induced by 27.5 mM dextrose was inhibited by all three beta blockers tested. The antioxidative and ER stress reducing effects of beta blockers were also observed in HepG2 cells.
Conclusions: The salutary effects of beta blockers on endothelial cells in reducing both ER stress and oxidative stress may contribute to the cardioprotective effects of these agents.
Background: Beta blockers are known to have favorable effects on endothelial function partly because of their capacity to reduce oxidative stress.
Methods and Results: To determine if beta blockers can also prevent dextrose-induced endoplasmic reticulum (ER) stress in addition to their anti-oxidative effects, human coronary artery endothelial cells and hepatocyte-derived HepG2 cells were treated with 27.5 mM dextrose for 24 hours in the presence of carvedilol (a lipophilic beta blockers with alpha blocking activity), propranolol (a lipophilic non selective beta blockers) and atenolol (a water-soluble selective beta blockers) and ER stress, oxidative stress and cell death were measured.
ER stress was measured using the placental alkaline phosphatase assay and western blot analysis of glucose regulated protein 78, c-jun-N-terminal kinase (JNK), phospho-JNK, eukaryotic initiating factor 2α (eIF2α) and phospho-eIF2α and measurement of X-box binding protein 1 (XBP1) mRNA splicing using reverse transcriptase-polymerase chain reaction. Superoxide (SO) generation was measured using the superoxide-reactive probe 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-A]pyrazin-3-one hydrochloride (MCLA) chemiluminescence. Cell viability was measured by propidium iodide (PI) staining method.
The ER stress, SO production and cell death induced by 27.5 mM dextrose was inhibited by all three beta blockers tested. The antioxidative and ER stress reducing effects of beta blockers were also observed in HepG2 cells.
Conclusions: The salutary effects of beta blockers on endothelial cells in reducing both ER stress and oxidative stress may contribute to the cardioprotective effects of these agents.

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