Effect of H11 Kinase/Hsp22 deletion in response to cardiac stress

The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress. We used microarray to examine differential gene expression by Hsp22 deletion at baseline and 3-day pressure overload. Left ventricles from wild type and Hsp22 knockout mice were selected from basal condition (each, n=3) and TAC surgery (each, n=4).小分子热休克蛋白（small molecular weight heat shock protein，Hsp）H11激酶/Hsp22（Hsp22）的表达仅局限于少数组织，在啮齿类动物和人类中均涵盖心脏与骨骼肌。本研究构建了小鼠基因敲除（knockout，KO）模型，探究了Hsp22在压力超负荷诱导的心肌肥厚中的调控作用。本研究比较了野生型（wild type，WT）与KO小鼠在基础状态及横主动脉缩窄（transverse aortic constriction，TAC）术后3天压力超负荷状态下的基因表达谱。上述研究数据揭示了Hsp22相关基因表达在心脏应激反应中的全新调控机制。本研究采用微阵列（microarray）技术，检测了基础状态与3天压力超负荷状态下Hsp22缺失所致的差异基因表达情况。本研究采集了基础状态下野生型与Hsp22基因敲除小鼠的左心室组织（每组各3例），以及TAC术后的对应左心室组织（每组各4例）。