ena-STUDY-UNIVERSITY OF BERN-11-06-2019-11:51:42:969-80
iPSC secretome alters metabolic pathway in IPF fibroblasts
Idiopathic Pulmonary fibrosis (IPF) is a chronic age related lung disease with high mortality. Age related perturbations cause elevated cellular stress that leads to mitochondrial dysfunction resulting in high susceptibility to lung injury and fibrosis. Secreted products of induced pluripotent stem cells (iPSC) iPSC-cm have anti-fibrotic mechanisms but their role in restoration of mitochondrial homeostasis in the lung injury is not known. To understand in details the antifibrotic mechanism of the iPSC secretome fibroblasts isolated from lung of IPF patients were treated with iPSC-cm and subjected to RNA sequencing. RNA seq revealed upregulation of genes involved in metabolic pathways after iPSC-cm treatment. The pathway analysis indicated towards restoration of cholesterol metabolism pathway after iPSC-cm treatment. Our data indicate that iPSC-cm restores dysfunctional metabolic pathways in the IPF fibroblast thus triggering mechanism that is essential for lung repair and regeneration.
Idiopathic Pulmonary fibrosis (IPF) is a chronic age related lung disease with high mortality. Age related perturbations cause elevated cellular stress that leads to mitochondrial dysfunction resulting in high susceptibility to lung injury and fibrosis. Secreted products of induced pluripotent stem cells (iPSC) iPSC-cm have anti-fibrotic mechanisms but their role in restoration of mitochondrial homeostasis in the lung injury is not known. To understand in details the antifibrotic mechanism of the iPSC secretome fibroblasts isolated from lung of IPF patients were treated with iPSC-cm and subjected to RNA sequencing. RNA seq revealed upregulation of genes involved in metabolic pathways after iPSC-cm treatment. The pathway analysis indicated towards restoration of cholesterol metabolism pathway after iPSC-cm treatment. Our data indicate that iPSC-cm restores dysfunctional metabolic pathways in the IPF fibroblast thus triggering mechanism that is essential for lung repair and regeneration.