Prostaglandin E2 inhibits pro-fibrotic function of human pulmonary fibroblasts by disrupting Ca2+-signaling

Purpose: Identification of gene expression in human lung fibroblasts, including analysis of impact of IPF (Idiopathic Pulmonary Fibrosis) as well as TGFß stimulation, with particular emphasis on prostanoid receptors and related pathways. Methods: Truseq stranded mRNA sequencing, via Illumina Hiseq 4000. Single reads, 75bp, ~25 million reads per sample. Quantification of gene expression in TPM using Kallisto, followed by Tximport. mRNA isolated via Qiagen RNeasy kit, with on-column DNase1 digestion. Results: Quantification of gene expression in primary human lung fibroblasts, including quantification of prostanoid GPCRs. Overall design: Transcriptomes of human lung fibroblasts (HPFs), assayed via RNA-seq for HPFs with/wo TGFß treatment, from normal donors and patients with IPF; n =3 for each group, with 4 groups.