Exon skipping of TGFβRI affects signalling and ECM expression in hypertrophic scar-derived fibroblasts.

ABSTRACT:

Background

In burn patients, wound healing is often accompanied by hypertrophic scar (HS) development, resulting in both functional and aesthetic problems. HSs are characterised by abundant presence of myofibroblasts that contribute to overproduction of extracellular matrix (ECM) that is regulated by the TGF-β signalling pathway. Studies have shown that inhibition of TGF-β receptors in fibrotic diseases reduces the fibrotic load. In the present study, we aim to inactivate ALK5, also known as TGF-β receptor I, in human HS fibroblasts by exon skipping using antisense oligonucleotides (AONs).

Methods

HS biopsies were used to isolate and set up fibroblast monocultures. AONs targeting ALK5 were supplemented to the fibroblast cultures to induce exon skipping, while pharmacological

SUBMITTER: Raktoe RS 

PROVIDER: S-EPMC7263111 | biostudies-literature | 2020 Jan-Dec

REPOSITORIES: biostudies-literature