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目的利用基因芯片技术筛选LPS诱导的急性肺损伤小鼠肺组织中与活化转录因子3(acting transcription factor 3,ATF3)相关的差异基因表达,以发现与ATF3可能相互作用的基因。方法采用基因芯片技术筛选野生型C57小鼠和ATF3敲基因小鼠经LPS处理后肺组织中的差异表达基因。进一步采用RT-PCR技术对重点基因的表达进行验证。结果与野生型C57小鼠比较,ATF3敲基因小鼠共筛选出1 692个差异基因,有21个与炎症调控相关的基因表达差异明显,其中,Myo18a、Mest、Gpr124、Rcan2、Tnfsf15、Ltbp3、Cdh2、Ppm1f、Spns2、Rarres2、Cgn、Mmrn2、Crb3、Adamts2、Mrc2、Sh3tc2、Cdk5rap1、Cenpf共18个基因在ATF3敲基因小鼠肺组织中表达明显上调;Padi4、Wfdc82个基因表达明显下调。对重点基因Tnfsf15(又称为TL1A)进一步验证,RT-PCR检测结果显示,表达趋势与基因芯片一致。结论 TL1A可能参与了ATF3对LPS诱导的急性肺损伤的炎症保护作用。
OBJECTIVE: To screen differentially expressed genes associated with activating transcription factor 3 (ATF3) in the lungs of mice with LPS-induced acute lung injury using gene chip technology to discover possible genes that interact with ATF3. Methods Gene microarray was used to screen differentially expressed genes in LPS-treated lungs of wild-type C57 mice and ATF3 knock-out mice. Further use of RT-PCR technology to verify the expression of key genes. Results Compared with wild type C57 mice, a total of 1 692 differential genes were found in ATF3 knockout mice, and 21 of them were significantly different from those in control group. Myo18a, Mest, Gpr124, Rcan2, Tnfsf15, Ltbp3, Eighteen genes of Cdh2, Ppm1f, Spns2, Rarres2, Cgn, Mmrn2, Crb3, Adamts2, Mrc2, Sh3tc2, Cdk5rap1 and Cenpf were significantly up-regulated in lung tissues of ATF3 knockout mice, while Padi4 and Wfdc82 genes were downregulated. The key gene Tnfsf15 (also known as TL1A) further validation, RT-PCR test results showed that the expression trend consistent with the gene chip. Conclusion TL1A may be involved in the protective effect of ATF3 on LPS-induced acute lung injury.