Gpr97 exacerbates AKI via mediating Sema3A signaling. Gpr97 exacerbates AKI via mediating Sema3A signaling

We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between the mice with renal IRI injury and sham-operated group.Expression of Gpr97 from this signature was quantified in the same kind of samples by real-time PCR, confirming the change pattern. By microarray analysis, we found that IR-induced Sema3A expression was significantly abolished by Gpr97 deficiency in mice Overall design: The kidney from wild type mice and Gpr97 deficiency mice with or without renal IRI injury were analysed.

本研究采用全基因组微阵列表达谱作为筛选平台，以鉴定能够区分肾缺血再灌注损伤（Renal Ischemia-Reperfusion Injury，简称IRI）小鼠与假手术组小鼠的差异基因。随后，本研究通过实时荧光定量PCR对该基因表达特征集中的Gpr97表达水平开展同类型样本的定量检测，验证了其表达变化趋势。经微阵列分析发现，Gpr97基因缺陷可显著抑制缺血再灌注诱导的小鼠Sema3A基因表达。实验设计概述：本研究分析了野生型小鼠与Gpr97基因缺陷小鼠在有无肾IRI损伤情况下的肾脏组织样本。