Project description:Single-nucleus RNA sequencing is an alternative to single-cell RNA sequencing with multiple advantages in terms of sample manipulation. However, benchmarking of this technique, particularly in the field of lung injury, is lacking. Here, we provide a comprehensive characterization of blemoycin-induced lung injury using whole mouse lungs profiled using single-nucleus RNA sequencing.
Project description:Sepsis is a serious systemic inflammatory reaction, which often leads to acute lung injury, and then affects lung function. This study aimed to explore the molecular mechanism of the interaction between il1b+ alveolar resident macrophages and pulmonary endothelial cells during sepsis induced lung injury using single-cell RNA sequencing technology.
Project description:Two single-cell RNA sequencing data sets were generated called "Whole lung" and "High Resolution". The "Whole lung" single-cell mRNAseq libraries were generated with Drop-Seq from whole mouse lungs upon bleomycin-induced injury and followed over time. Samples were taken at days 3 (n = 3), 7 (n = 5), 10 (n = 3), 14 (n = 4), 21 (n = 4) and 28 (n = 2). Control samples (n = 7) were administered saline only, also indicated with PBS or day0. The "High resolution" single-cell mRNAseq libraries were generated with Drop-Seq from the epithelial compartment of mouse lungs upon bleomycin-induced injury and followed over time. Samples were taken daily for two weeks and at days 21, 28, 36, 54 after injury. Control samples (n = 2) were administered saline only, also indicated with PBS or day0.
Project description:Yangyinqingfei Decoction (YYQFD), a traditional Chinese prescription, is well known in the treatment of diphtheria and lung-related diseases in clinic. However, the underlying mechanism how to treat lung-related diseases remains unclear. In the present study, the intervention effect of YYQFD on PM2.5-induced lung injury mice and its potential mechanism were investigated by metabolomics and proteomic techniques. The results showed that YYQFD could significantly improve pulmonary functions, relieve lung injury, as well as reduce IL-6, TNF-α and MDA, and increase SOD levels in serum and BALF of PM2.5-induced lung injury mice. Furthermore, the protein-metabolite joint analysis presented that YYQFD regulated the pathways of arachidonic acid metabolism, linoleic acid metabolism, and biosynthesis of unsaturated fatty acids with significantly down-regulating arachidonic acid, 20-HETE, prostaglandin E2, lecithin, linoleic acid, α-linolenic acid, eicosatetraenoic acid, and γ-linolenic acid, and up-regulating PTGES2, GPX2 and CBR3 protein expressions in lung tissue. A regulatory metabolic network map was further constructed, which provide us a better understanding about the role of YYQFD on PM2.5-induced lung injury mice and new insight into YYQFD application for the treatment of lung-related diseases.
Project description:Data analyzed proteins extracted from lung tissue samples from OA-induced acute lung injury model rats.
Samples were collected at 0 (pretreatment), 3, 6,
24, 48, 96 h after OA administration. Whole tissue extracts were prepared from three individuals and analyzed using the DIA-MS method.
Project description:This study investigates the role of GRP75 (Hspa9)-mediated mitochondria-associated membranes (MAMs) in SARS-CoV-2 nucleocapsid (N) protein-induced acute lung injury. Using single-cell RNA sequencing of lung macrophages from control and GRP75 knockdown mice, we demonstrate that N protein promotes GRP75-dependent ER-mitochondria tethering, leading to mitochondrial calcium overload and proinflammatory macrophage activation. GRP75 knockdown attenuates N protein-induced lung injury by reprogramming alveolar macrophage identity from a pro-inflammatory Car4+ state to a metabolically quiescent Hspa9-low state.