Transcription profiling by array of mouse main branch pulmonary artery to study the differences between wild type and miR-145 KO mice exposed to normoxic or hypoxic conditions

Hypoxia is used as a model for pulmonary arterial hypertension. MiR-145 is upregulated in pulmonary arterial hypertension in humans and female mice. It has been observed that miR-145 knock out mice have reduced vascular remodelling in response to hypoxia. Therefore, knock down of miR-145 could be used as a therapy for pulmonary arterial hypertension in humans. This microarray has helped us to elucidate some of the pathways in the miR-145 knock out mice that may protect against vascular remodelling. Wild type (WT) mice and homozygous miR-145 -/- female mice (strain C57BL6J/129SVEV) at 8 weeks old were exposed to chronic hypoxia for 2 weeks or maintained in normoxic conditions and pulmonary arteries were dissected at 10 weeks of age. This study contained 4 groups, WT hypoxic, WT normoxic, miR-145 -/-, hypoxic miR-145 -/- normoxic each containing 6 animals. All adjacent comparisons were made to analyze the data (a 2 by 2 design).缺氧被用作肺动脉高压（pulmonary arterial hypertension）的研究模型。MiR-145在人类及雌性小鼠的肺动脉高压病变组织中呈高表达状态。已有研究发现，MiR-145基因敲除小鼠在缺氧刺激下的血管重构程度显著降低。因此，敲低MiR-145或可成为人类肺动脉高压的潜在治疗手段。本次基因芯片（microarray）实验旨在阐明MiR-145基因敲除小鼠体内可能参与抵御血管重构的相关信号通路。 选取8周龄的野生型（Wild type, WT）小鼠与纯合子MiR-145基因敲除（miR-145 -/-）雌性小鼠（品系为C57BL6J/129SVEV），将其分为两组：一组置于慢性缺氧环境中饲养2周，另一组维持于常氧环境；待小鼠至10周龄时，分离获取其肺动脉组织。本研究共设置4个实验组：野生型缺氧组、野生型常氧组、MiR-145基因敲除缺氧组、MiR-145基因敲除常氧组，每组各包含6只实验动物。数据分析采用2×2实验设计方案，对各组进行两两相邻比较以完成数据解析。