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首页> 外文期刊>American Journal of Physiology >Bioinformatic identification of novel early stress response genes in rodent models of lung injury.
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Bioinformatic identification of novel early stress response genes in rodent models of lung injury.

机译：啮齿动物肺损伤模型中新的早期应激反应基因的生物信息学鉴定。

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Acute lung injury is a complex illness with a high mortality rate (>30%) and often requires the use of mechanical ventilatory support for respiratory failure. Mechanical ventilation can lead to clinical deterioration due to augmented lung injury in certain patients, suggesting the potential existence of genetic susceptibility to mechanical stretch (6, 48), the nature of which remains unclear. To identify genes affected by ventilator-induced lung injury (VILI), we utilized a bioinformatic-intense candidate gene approach and examined gene expression profiles from rodent VILI models (mouse and rat) using the oligonucleotide microarray platform. To increase statistical power of gene expression analysis, 2,769 mouse/rat orthologous genes identified on RG_U34A and MG_U74Av2 arrays were simultaneously analyzed by significance analysis of microarrays (SAM). This combined ortholog/SAM approach identified 41 up- and 7 downregulated VILI-related candidate genes, results validated by comparable expression levels obtained by either real-time or relative RT-PCR for 15 randomly selected genes. K-mean clustering of 48 VILI-related genes clustered several well-known VILI-associated genes (IL-6, plasminogen activator inhibitor type 1, CCL-2, cyclooxygenase-2) with a number of stress-related genes (Myc, Cyr61, Socs3). The only unannotated member of this cluster (n = 14) was RIKEN_1300002F13 EST, an ortholog of the stress-related Gene33/Mig-6 gene. The further evaluation of this candidate strongly suggested its involvement in development of VILI. We speculate that the ortholog-SAM approach is a useful, time- and resource-efficient tool for identification of candidate genes in a variety of complex disease models such as VILI.
机译：急性肺损伤是一种高死亡率（> 30％）的复杂疾病，通常需要使用机械通气支持来治疗呼吸衰竭。由于某些患者的肺损伤加剧，机械通气可导致临床恶化，这表明遗传对机械拉伸的易感性（6、48），其性质尚不清楚。为了鉴定受呼吸机诱导的肺损伤（VILI）影响的基因，我们利用生物信息学上的候选基因方法，并使用寡核苷酸微阵列平台检查了啮齿动物VILI模型（小鼠和大鼠）的基因表达谱。为了提高基因表达分析的统计能力，同时通过微阵列重要性分析（SAM）同时分析了RG_U34A和MG_U74Av2阵列上鉴定的2,769个小鼠/大鼠直系同源基因。这种组合的直向同源物/ SAM方法鉴定了41个上调和7个下调的VILI相关候选基因，该结果通过实时或相对RT-PCR获得的15种随机选择基因的可比表达水平得到了验证。 48个VILI相关基因的K均值聚类将几个著名的VILI相关基因（IL-6，纤溶酶原激活物抑制剂1型，CCL-2，环氧合酶-2）与许多与压力相关的基因（Myc，Cyr61）聚类，Socs3）。该簇中唯一未注释的成员（n = 14）是RIKEN_1300002F13 EST，这是与压力相关的Gene33 / Mig-6基因的直系同源基因。对该候选人的进一步评估强烈表明其参与了VILI的发展。我们推测，ortholog-SAM方法是一种有用的，节省时间和资源的工具，可用于识别多种复杂疾病模型（例如VILI）中的候选基因。

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