Project description:There were similarities in the microRNA expression profiles in sheep model and idiopathic pulmonary fibrosis (IPF) suggest that bleomycin induced lung injuries share similar molecular mechanisms associated with the disease IPF
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
Project description:Idiopathic pulmonary fibrosis (IPF) is a type of pulmonary fibrosis, a disease that results in scarring and stiffness of lung tissue affecting over 5 million people globally, while the underlying disease mechanisms in IPF are largely unknown. As an animal model of IPF, a single intratracheal injection of bleomycin (BLM) is generally employed, in which cell death of type II alveolar epithelial cells (AEC II) is a trigger of pulmonary fibrosis. One of mitogen-activated protein kinases, p38 is well known as an important regulator of inflammatory responses and cell fate such as apoptosis, differentiation and tumorgenesis. Given that mice with different intrinsic activity of p38 in AEC II were subjected to BLM instillation and investigated, candidate genes in the development of pulmonary fibrosis would be screened. Here, we provide gene expression profiling of lung tissues using the RNA sequencing for identifying changes in gene expression.
Project description:Lung resident mesenchymal stem cells exert a pivotal role in tissue repair. Idiopathic pulmonary fibrosis is characterized by an aberrant tissue repair. We performed a transcriptomic analysis to characterize lung resident mesenchymal stem cells from idiopathic pulmonary fibrosis patients
Project description:This study aimed to delineate molecular phenotypes of the lung microenvironment across idiopathic interestitial pneumonias, namely interstitial pneumonia with autoimmune features (IPAF)and idiopathic pulmonary fibrosis (IPF) through proteomic analysis of bronchoalveolar lavage fluid (BALF).
Project description:In summary, we characterized the role of m6A modification in pulmonary fibrosis. We reveal that m6A modification is increased in bleomycin induced pulmonary fibrosis mice model, FMT-derived myofibroblasts and idiopathic pulmonary fibrosis patient lung samples. Lowering m6A level through silencing METTL3 suppress FMT process in vitro and vivo. Fundamentally, m6A modification regulates FMT by modulating the translation of KCNH6 mRNA in a YTHDF1 dependent manner. This study provides novel insights into the mechanism of FMT process and suggests m6A modification intervention may be a promising therapeutic strategy for pulmonary fibrosis.
