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Abstract：
Physiological and pathological cardiomyocyte hypertrophy are important pathophysiological processes of adult congenital heart disease-associated ventricular hypertrophy. Glutamic oxaloacetic transaminase (GOT) is a vital marker of myocardial injury. This study aimed to investigate the changes in GOT levels during physiological and pathological cardiomyocyte hypertrophy in rats.
RNA-seq analysis and colorimetric methods were used to evaluate the changes in GOT mRNA and activity, respectively. GOT2 protein expression was detected by western blotting and immunofluorescence. Hematoxylin-eosin and wheat germ agglutinin methods were used to observe changes in rat cardiomyocyte morphology.
In juvenile rat hearts, GOT mRNA expression and activity, and GOT2 protein level increased with age-related physiological cardiomyocyte hypertrophy; however, GOT2 protein level was reduced in hypoxia-induced pathological cardiomyocyte hypertrophy.
GOT2 may regulate physiological and pathological myocardial hypertrophy in rats. We speculated that the low GOT2 level contributed to the rapid occurrence of pathological cardiomyocyte hypertrophy, causing strong plasticity of right ventricular cardiomyocytes in the early postnatal period and heart failure in adulthood.
RNA-seq analysis and colorimetric methods were used to evaluate the changes in GOT mRNA and activity, respectively. GOT2 protein expression was detected by western blotting and immunofluorescence. Hematoxylin-eosin and wheat germ agglutinin methods were used to observe changes in rat cardiomyocyte morphology.
In juvenile rat hearts, GOT mRNA expression and activity, and GOT2 protein level increased with age-related physiological cardiomyocyte hypertrophy; however, GOT2 protein level was reduced in hypoxia-induced pathological cardiomyocyte hypertrophy.
GOT2 may regulate physiological and pathological myocardial hypertrophy in rats. We speculated that the low GOT2 level contributed to the rapid occurrence of pathological cardiomyocyte hypertrophy, causing strong plasticity of right ventricular cardiomyocytes in the early postnatal period and heart failure in adulthood.
摘要：
背景：生理和病理性心肌细胞肥大是成人先天性心脏病相关心室肥大的重要病理生理过程。谷草转氨酶(GOT)是心肌损伤的重要标志。本研究旨在探讨大鼠生理性和病理性心肌细胞肥大过程中GOT水平的变化。
方法：RNA-seq分析和比色法用于评估GOTmRNA和活性的变化，分别。通过蛋白质印迹和免疫荧光检测GOT2蛋白的表达。采用苏木精-伊红和麦胚凝集素方法观察大鼠心肌细胞形态的变化。
结果：在幼鼠心脏中，GOTmRNA表达和活性，和GOT2蛋白水平随着年龄相关的生理性心肌细胞肥大而增加；然而，在缺氧诱导的病理性心肌细胞肥大中，GOT2蛋白水平降低。
结论：GOT2可调节大鼠生理性和病理性心肌肥厚。我们推测，低GOT2水平有助于病理性心肌细胞肥大的快速发生，在出生后早期引起右心室心肌细胞的强可塑性和成年后的心力衰竭。
方法：RNA-seq分析和比色法用于评估GOTmRNA和活性的变化，分别。通过蛋白质印迹和免疫荧光检测GOT2蛋白的表达。采用苏木精-伊红和麦胚凝集素方法观察大鼠心肌细胞形态的变化。
结果：在幼鼠心脏中，GOTmRNA表达和活性，和GOT2蛋白水平随着年龄相关的生理性心肌细胞肥大而增加；然而，在缺氧诱导的病理性心肌细胞肥大中，GOT2蛋白水平降低。
结论：GOT2可调节大鼠生理性和病理性心肌肥厚。我们推测，低GOT2水平有助于病理性心肌细胞肥大的快速发生，在出生后早期引起右心室心肌细胞的强可塑性和成年后的心力衰竭。
