FibroDB: Expression Analysis of Protein-Coding and Long Non-Coding RNA Genes in Fibrosis

Abstract

Most long non-coding RNAs (lncRNAs) are expressed at lower levels than protein-coding genes and their expression is often restricted to specific cell types, certain time points during development, and various stress and disease conditions, respectively. To revisit this long-held concept, we focused on fibroblasts, a common cell type in various organs and tissues. Using fibroblasts and changes in their expression profiles during fibrosis as a model system, we show that the overall expression level of lncRNA genes is significantly lower than that of protein-coding genes. Furthermore, we identified lncRNA genes whose expression is upregulated during fibrosis. Using dermal fibroblasts as a model, we performed loss-of-function experiments and show that the knockdown of the lncRNAs LINC00622 and LINC01711 result in gene expression changes associated with cellular and inflammatory responses, respectively. Since there are no lncRNA databases focused on fibroblasts and fibrosis, we built a web application, FibroDB, to further promote functional and mechanistic studies of fibrotic lncRNAs.

Integrative Analysis of Angiogenesis-Related Long Non-Coding RNA and Identification of a Six-DEARlncRNA Signature Associated with Prognosis and Therapeutic Response in Esophageal Squamous Cell Carcinoma

“…Xu et al revealed that LINC01711 was upregulated in esophageal carcinoma and associated with malignant phenotypes and poor prognosis [ 42 ]. Existing literature had shown that LINC01711 was included in the prognostic model and may play essential roles in malignant progression of ESCC, triple negative breast cancer and fibrosis [ 43 , 44 , 45 ]. Shi et al reported that AC011997.1 was considered as a prognostic risk factor in ESCC [ 30 ].…”

Long Non-Coding RNAs in Cardiac and Pulmonary Fibroblasts and Fibrosis

“…As for fibrotic lncRNAs, especially in the cardiopulmonary system and its associated diseases, the number of functionally characterized fibrotic lncRNAs is scarce. To assist in the identification of lncRNAs expressed in fibroblasts and involved in fibrosis-especially in cardiac and pulmonary fibrosis-we recently released the web application FibroDB [86] (https://rnamedicine.shinyapps.io/FibroDB/, accessed on 12 July 2022).…”

Dextromethorphan inhibits collagen transport in the endoplasmic reticulum eliciting an anti-fibrotic response inex-vivoandin vitromodels of pulmonary fibrosis

“…0.05) changed their abundance upon TGFb1 treatment (Figure 3A). Pathway enrichment analysis of these significantly regulated proteins showed enrichment of pro-fibrotic pathways 22,23 such as ECM organisation, Cell Adhesion and Tissue morphogenesis (Figure 3B). TGFb1 treatment caused a significant upregulation of pro-fibrotic ECM proteins 24 such as COL1, COL3, FN1, THBS1, FBN1 (Figure 3B) and an upregulation of enzymes that aid the polymerization of collagens in ECM such as BMP1, LOXL2, COL5 25 .…”