Expression data from young (4 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. 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（GRK2）现已被确立为心脏功能与心肌结构的关键调控因子。人类心力衰竭与心肌缺血患者的心脏组织中GRK2水平升高，而在上述病症的动物模型中，对GRK2进行基因抑制可产生心脏保护作用。然而，这些保护效应背后的分子机制尚未完全明确。我们选用成年GRK2半合子小鼠（GRK2+/-）作为研究模型，以评估持续性全身抑制GRK2对衰老过程中心脏组织的影响。我们通过基因芯片技术，解析了GRK2半合子小鼠心脏保护作用背后的全局基因表达调控程序。我们收集了4月龄小鼠的心脏组织用于RNA提取，并在Affymetrix基因芯片上完成杂交实验。