Exosomal lncRNA TCONS_00064356 derived from injured alveolar epithelial type II cells affects the biological characteristics of mesenchymal stem cells.

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disease, and a leading cause of morbidity and mortality worldwide. There is still a lack of effective treatment to improve pulmonary structural abnormality and reverse the progression of COPD. Mesenchymal stem cell (MSC)-based therapies have attracted much attention and show promising clinical application prospects in COPD treatment. Understanding the communication between injured alveolar cells and MSCs will help us improve the efficiency of MSC-based therapies. Here, we showed that exosomes secreted by injured alveolar epithelial type II (AEC-II) cells could promote the proliferation and migration of MSCs, accompanied with increased expression levels of genes related to mitochondrial synthesis and transfer. Moreover, we identified 21 significantly dysregulated exosomal lncRNAs (16 upregulated and 5 downregulated) using lncRNA sequencing. In addition, we found that lncRNA TCONS_00064356-overexpressing MSCs showed increased proliferation and migration capacities and upregulated expression levels of the genes related to mitochondrial synthesis and transfer. Together, our study uncovers a new potential exosome-mediated communication pathway between injured AEC-II cells and MSCs and provides new targets and ideas for improving the efficiency of MSC-based therapies for COPD.