Project description:We sequenced more than 13000 cells of the pleuroperitoneal folds of a mouse embryo to better understand the mosaic nature of the developing diaphragm. We identified 18 different clusters, and 10 unique cell types. Through our analysis, we were able to determine that most of the developing diaphragm is comprised of mesenchymal cells, and that genes necessary for proper diaphragm development are expressed in these types of cells. These observations provide a strong basis for furhter studies about the development and physiology of the diaphragm.
Project description:Mechanical ventilation contributes to diaphragm atrophy and muscle weakness, which is referred to as ventilator-induced diaphragmatic dysfunction (VIDD).Through snRNA seq, we demonstrated that diaphragm fibrosis resulting from FAP proliferation, EMT, immune cell infiltration, and diaphragm atrophy which are induced by phrenic nerve ending loss are the underlying causes of VIDD.
Project description:Purpose: The goal of this study is to determine what genes are expressed, and at what level, in the developing diaphragm at a timepoint shown to be critical in the initiation of congenital diaphragmatic hernias in mice. Methods: PPFs were dissected from staged mouse embryos Methods: summary Purpose: The goal of this study is to determine what genes are expressed, and at what level, in the developing diaphragm at a timepoint shown to be critical in the initiation of congenital diaphragmatic hernias in mice. Methods: PPFs were dissected from staged mouse embryos
Project description:We characterized gene expression changes in the developing mouse liver at gestational days (GD) 11.5, 12.5, 13.5, 14.5, 16.5, and 19.5 and in the neonate (postnatal day (PND) 7 and 30) using full-genome microarrays and compared these changes to that in the adult liver. The fetal liver, and to a lesser extent the neonatal liver, exhibited dramatic differences in gene expression compared to adults. Canonical pathway analysis of the fetal liver signature demonstrated increases in functions important in cell replication and DNA fidelity whereas most metabolic pathways of intermediary metabolism were suppressed. Comparison of the dataset to a number of previously published datasets revealed 1) a striking similarity between the fetal liver and that of the pancreas in both mice and humans, 2) a nucleated erythrocyte signature in the fetus and 3) suppression of most xenobiotic metabolism genes throughout development, except a number of transporters associated with expression in hematopoietic cells. Keywords: gene expression/microarray We characterized gene expression changes in the developing mouse liver at gestational days (GD) 19 and in the neonate (postnatal day (PND) 7 and 30) using full-genome microarrays and compared these changes to that in the adult liver. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Mouse 430 2.0 GeneChips. Data from 16 samples, with four mice in each of the four age groups, were analyzed.
Project description:The retention of galactose-deficient IgA1 (Gd-IgA1) in the glomerular mesangium is a hallmark of IgA nephropathy (IgAN). The immune complex formed by Gd-IgA1 binds to transferrin receptor 1 (TfR1) and deposits on mesangial cell, inducing cell proliferation, inflammatory response, matrix secretion, etc., causes organic damage and dysfunction of the kidney. Even though, the mechanism of how Gd-IgA1 recognize and bind to TfR1 is unclear. In this experiment, we ami to determine the specific interaction region responsible for Gd-IgA1 and TfR1. We prepared a complex of Gd-IgA1 and TfR1 by incubating the two proteins under acidic conditions and stabilizing it using the chemical cross-linking agent glutaraldehyde. And then, the gel bands corresponding to the Gd-IgA1-TfR1 complex was exexcised from the SDS-PAGE gel and analyzed by high-resolution mass spectrometry. This analysis identified fragments containing the hinge peptide sequence, with the R276 residue interacting with the E350 and D356 residues in the apical domain of TfR1. Our results reveal that the hinge peptide of Gd-IgA1 interacts specifically with the apical domain of TfR1.
Project description:Single cell RNA-seq study of T lymphocyte differentiation WT and LAT deficient mice in order to deciphy gd T-cell lineage commitment.
Project description:Single cell RNA-seq study of T lymphocyte differentiation WT and LAT deficient mice in order to deciphy gd T-cell lineage commitment.