ABSTRACT
This study demonstrated that ARID5B mRNA is present in mouse cardiomyocyte HL-1 cells, and that ARID5B siRNA constantly knocked down ARID5B gene expression to the 40% level of control. AMPKα2 protein was elevated in such ARID5B knockdown HL-1 cells, and this was accompanied by an increase in the level of phosphorylated AMPKα. Since AMPKα2 mRNA levels did not change in ARID5B knockdown cells, the stability of AMPKα2 protein was investigated using inhibitors for protein synthesis and proteasomal degradation. Treatment of HL-1 cells with either cycloheximide or MG132 caused an appreciable increase in the amount of AMPKα2 protein in ARID5B knockdown cells, which suggests that knockdown of ARID5B mRNA extends the half-life of AMPKα2 protein in HL-1 cells via yet unidentified mechanisms. As for the expected downstream consequences of AMPKα2 activation, we found thus far that glucose uptake, fatty acid uptake, or fatty acid oxidation remained unchanged in HL-1 cells after knockdown of ARID5B. Further studies are required to understand the mechanisms for ARID5B knockdown and resulting AMPKα2 activation, and also to identify which metabolic pathways are affected by AMPKα2 activation in these cells. In summary, this study provided the foundation for an in vitro cell culture system to study possible roles of ARID5B in cardiomyocytes.
Subject(s)
AMP-Activated Protein Kinases/metabolism , DNA-Binding Proteins/physiology , Myocytes, Cardiac/metabolism , Transcription Factors/physiology , Animals , Cell Line , Cycloheximide/pharmacology , DNA-Binding Proteins/genetics , DNA-Binding Proteins/metabolism , Fatty Acids/metabolism , Gene Knockdown Techniques , Glucose/metabolism , Leupeptins/pharmacology , Male , Mice , Myocardium/metabolism , Oxidation-Reduction , Phosphorylation , RNA, Messenger/metabolism , Signal Transduction , Transcription Factors/genetics , Transcription Factors/metabolismABSTRACT
Acute myocardial infarction (AMI) during pregnancy or in the early postpartum period is a rare event but may cause perinatal morbidity and mortality. Early diagnosis of AMI is critical for appropriate treatment. We report a case of postpartum AMI in a 40-year-old multiparous woman with varicose veins. On postpartum day 3, the patient suffered severe chest pain. She had been administered oral methylergometrine. In addition to ST-segment elevation in her electrocardiogram, the patient presented with a positive result on whole blood rapid panel tests for troponin T and heart-type fatty acid-binding protein (H-FABP). These findings indicated AMI in the anterolateral wall. The chest pain disappeared with the prompt administration of intravenous pentazocine hydrochloride and sublingual nitroglycerin spray. Angiography did not reveal any signs of coronary stenosis. To our knowledge, this is the first report of postpartum AMI diagnosed rapidly with combined use of troponin T and H-FABP qualitative panel tests.
