HAMSCs regulate EMT in the progression of experimental pulmonary fibrosis through delivering miR-181a-5p targeting TGFBR1.

ABSTRACT:

Background

Pulmonary fibrosis (PF) is a common and multidimensional devastating interstitial lung disease. The development of novel and more effective interventions for PF is an urgent clinical need. A previous study has found that miR-181a-5p plays an important role in the development of PF, and human amniotic mesenchymal stem cells (hAMSCs) exert potent therapeutic potential on PF. However, whether hAMSCs act on PF by delivering miR-181a-5p and its detailed mechanism still remain unknown. Thus, this study was designed to investigate the underlying possible mechanism of hAMSCs on PF in bleomycin (BLM)-induced mouse PF model, and a co-culture system of hAMSCs and A549 cells epithelial mesenchymal transition (EMT) model, focusing on its effects on collagen deposition, EMT, and epith

SUBMITTER: Wang Y 

PROVIDER: S-EPMC11702096 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature