Central Laboratory, Jilin University Second Hospital, Changchun, PR China.
Biochemistry (Mosc). 2011 Oct;76(10):1140-6. doi: 10.1134/S0006297911100075.
The individual signaling pathways underlying cardiac hypertrophy, which is induced by either α or β adrenergic receptor (AR), are different. Activation of different AR subtypes couples to different G proteins and induction of specific signaling pathways, which ultimately results in subtype-specific regulation of cardiac function. We present the first proteomics study identifying proteins that are related to AR subtype-specific hypertrophy in cardiomyocytes by comparing the two-dimensional electrophoresis patterns between neonatal rat cardiomyocytes treated by phenylepinephrin (PE) and by isoproterenol (ISO). An improved 2-DE strategy was used in these comparative experiments. Twenty-five differentially expressed proteins in cardiomyocytes treated by PE or treated by ISO were successfully analyzed and identified using matrix-assisted laser desorption/ionization-time of flight mass spectrometry, especially those that might be responsible to intracellular oxidative stress such as dismutase, peroxiredoxin, and thioredoxin-like protein p46. In addition, induced reactive oxygen species were also found to be AR subtype-specifically relevant to endoplasmic reticulum proteinase ERK1/2 phosphorylation during the development of hypertrophy induced by different AR subtypes. The results will help to better understand the underlying mechanisms of different adrenergic receptor subtype-induced hypertrophy.
心脏肥厚是由α或β肾上腺素受体（AR）引起的，其背后的个体信号通路是不同的。不同 AR 亚型的激活与不同的 G 蛋白偶联，并诱导特定的信号通路，最终导致心脏功能的亚型特异性调节。我们通过比较苯肾上腺素（PE）和异丙肾上腺素（ISO）处理的新生大鼠心肌细胞的二维电泳图谱，进行了首次蛋白质组学研究，以确定与 AR 亚型特异性肥厚相关的蛋白。在这些比较实验中使用了改进的 2-DE 策略。使用基质辅助激光解吸/电离飞行时间质谱法成功分析和鉴定了 PE 或 ISO 处理的心肌细胞中 25 种差异表达的蛋白质，特别是那些可能与细胞内氧化应激有关的蛋白质，如超氧化物歧化酶、过氧化物酶和硫氧还蛋白样蛋白 p46。此外，还发现诱导的活性氧物质在不同 AR 亚型诱导的肥厚发展过程中与内质网蛋白激酶 ERK1/2 磷酸化具有 AR 亚型特异性相关性。这些结果将有助于更好地理解不同肾上腺素能受体亚型诱导的肥厚的潜在机制。
