Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

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 in GRK2 hemizygous mice. 9 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。人类心力衰竭及缺血性病变患者的心脏组织中GRK2水平显著升高，而在对应病理的动物模型中，抑制GRK2的基因表达可发挥心脏保护作用，但上述保护效应的分子机制尚未完全阐明。我们采用成年GRK2半合子小鼠（GRK2+/-）作为模型，评估持续全身性抑制GRK2对不同年龄阶段心脏组织的影响。为解析GRK2半合子小鼠心脏保护效应背后的全基因组基因表达程序，我们借助基因芯片（microarrays）技术开展实验：采集9月龄小鼠的心脏组织用于RNA提取，随后在Affymetrix基因芯片上完成杂交实验。