Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice

G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection with age in GRK2 hemizygous mice in comparison with their wild-type littermates. 9 month-old and 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.G蛋白偶联受体激酶2（G protein-coupled receptor kinase 2，GRK2）现已被证实为心脏功能与心肌结构的关键调控因子。人类心力衰竭与缺血病症中，心脏组织内的GRK2水平升高；而在上述病理的动物模型中，对GRK2实施基因抑制可发挥心脏保护作用。然而，这些效应背后的分子机制尚未完全阐明。本研究选用成年GRK2半合子小鼠（GRK2+/-）作为实验模型，用以评估系统性持续抑制GRK2对衰老过程中心脏组织的影响。我们借助微阵列（microarrays）技术，对比GRK2半合子小鼠与其野生型同窝幼鼠，解析衰老状态下介导心脏保护作用的全基因表达程序。研究收集了9月龄与4月龄小鼠的心脏组织，用于RNA提取，并开展Affymetrix微阵列杂交实验。