Whole transcriptome analysis of control human fibroblasts, TGFß-induced human fibroblasts, and fibroblasts co-cultured with normal lung decellularized scaffolds and fibroblasts co-cultured with bleomycin-induced lung decellularized scaffolds.
Fibrosis refers to the abnormal proliferation and excessive accumulation of fibrous tissue in an organ or tissue, typically caused by chronic injury or inflammation. Fibroblasts play a crucial role in the initiation and progression of fibrosis, with their excessive activation and overproduction of ECM being key mechanisms in fibrotic diseases. In this study, we constructed decellularized lung scaffolds from normal mice and bleomycin-induced lung decellularized scaffolds to analyze and compare the differential gene expression in control human fibroblasts, TGFß-induced human fibroblasts, fibroblasts co-cultured with normal lung decellularized scaffolds, and fibroblasts co-cultured with bleomycin-induced lung decellularized scaffolds. This investigation aims to explore the impact of ECM on fibroblast activation and its underlying mechanisms. Overall design: We divided human fibroblasts into four groups: control group, TGFß-induced group, co-culture with normal lung decellularized scaffold group, and co-culture with bleomycin-induced lung decellularized scaffold group. After three days of co-culture, RNA was extracted from the human fibroblasts.