Fig. 4

Molecular profiling by RNA-sequencing reveals that Tem1 deficiency in mice mitigates stretch-mediated fibrosis and inflammation during scar progression. A The scar tissues from Tem1^WT/WT and Tem1^lacZ/lacZ mice with or without traction force (n = 3 for each group) is subjected to RNA-sequencing. Principal component analysis reveals distinct changes across four groups. B Canonical pathways are analyzed by IPA software following DEGs. C Cell type inference for each group is predicted by xCell software. D Cluster methods are conducted by the tidyverse package to explore gene expression patterns. The gene ontology biological processes of DEGs in each cluster are analyzed by the clusterProfiler package. Tem1^WT/WT mice without traction force (sham group), WTSH; Tem1^lacZ/lacZ mice without traction force (sham group), lacZSH; Tem1^WT/WT mice with traction force (traction group), WTTR; Tem1^lacZ/lacZ mice with traction force (traction group), lacZTR