Expression data of stimulated murine primary lung fibroblasts

Pulmonary fibrosis (PF) is both an independent disease and a pathologic basis for fibroproliferative lung diseases. Understanding of underlying mechanisms of PF is critical for developing effective therapeutics. Fibroblasts activation and extracellular matrix deposition are critical in pathogenesis of PF. Stimulation of certain factors can induce profibrotic changes in fibroblasts. Evaluation of associated genes in treated fibroblasts is helpfu to analyze the profibrotic changes of this critical effector cell for PF. We used microarrays to detail the global programme of gene expression following TGFβ and CCL1 stimulation of primary lung fibroblasts. Primary lung fibroblasts were isolated from murine lungs. We treated the cells with the classic profibrotic factor TGFβ as the positive control and CCL1 in triplicates.These stimulated samples as well as untreated fibroblasts were collected for RNA extraction and hybridization on Affymetrix microarrays.

肺纤维化（Pulmonary fibrosis, PF）既是一类独立疾病，也是肺纤维增生性疾病的病理基础。阐明肺纤维化的潜在发病机制，对于开发有效治疗手段至关重要。成纤维细胞（fibroblasts）活化与细胞外基质沉积，是肺纤维化发病进程中的关键环节。特定因子的刺激可诱导成纤维细胞发生促纤维化表型改变。对经因子处理的成纤维细胞中的关联基因进行分析，有助于解析这类肺纤维化关键效应细胞的促纤维化变化。我们采用基因芯片（microarrays）技术，详细解析了原代肺成纤维细胞（primary lung fibroblasts）经转化生长因子β（transforming growth factor β, TGFβ）与趋化因子配体1（chemokine (C-C motif) ligand 1, CCL1）刺激后的全基因组基因表达谱变化。原代肺成纤维细胞从小鼠肺部分离得到。我们以经典促纤维化因子转化生长因子β作为阳性对照，并设置3个生物学重复开展趋化因子配体1刺激处理。收集上述经因子刺激的样本以及未处理的成纤维细胞，进行RNA提取，并在Affymetrix基因芯片上完成杂交实验。