Project description:To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg Cells were FACS sorted based upon expression of CD4, Foxp3 and expression of Nrp1.
Project description:Obesity gives rise to metabolic complications by mechanisms that are poorly understood. While chronic inflammatory signaling in adipose tissue is typically associated with metabolic deficiencies linked to excessive weight gain, we identified a subset of NRP1-expressing myeloid cells that accumulate in adipose tissue and protect against obesity and metabolic syndrome. Ablation of NRP1 in macrophages compromised lipid uptake in these cells, which reduced substrates for fatty acid β-oxidation and shifted energy metabolism of these macrophages towards a more inflammatory glycolytic metabolism. Conditional deletion of NRP1 in LysM Cre-expressing cells lead to inadequate adipose vascularization, accelerated weight gain and reduced insulin sensitivity even independent of weight gain. Transfer of NRP1+ hematopoietic cells improved glucose homeostasis, resulting in the reversal of a prediabetic phenotype. Our findings suggest a pivotal role for adipose tissue resident NRP1+-expressing macrophages in driving healthy weight gain and maintaining glucose tolerance.
Project description:In order to stablish differences between M. tuberculosis gene expression when different growth conditions are used in a macrophage infection model (Log, NRP1 and NRP2 stages), we have designed a whole M. tb genome microarray combined with 173 human genes. RNA from bacilli and macrophages was isolated at 24h and 48h post infection. Microarrays were hybridized usign a combination of mycobacterial and human RNA and expression level was assesed using the Agilent SureScan Microarray Scanner. Then, data were normalized and differential expression was analyzed.
Project description:Triple-negative breast cancers (TNBC) are a particularly aggressive breast cancer subtype with poor prognosis and high relapse rates. Due to a lack of identified targeted therapies, chemotherapy currently remains as the primary treatment for TNBC. Approximately 25-39% of TNBC are claudin-low breast cancers, which are mainly defined by low expression of cell-cell adhesion proteins and enrichment of mesenchymal signatures. Functional studies have demonstrated the potential role of the transmembrane-coreceptor, Neuropilin-1 (NRP1) in regulating the progression of these tumours. However, there have been no high-throughput studies to date that comprehensively investigate NRP1-modulated cell signalling across multiple claudin-low cell lines. Therefore, we knocked-down NRP1 by two small-interfering RNA (siRNA) or two short-hairpin RNA (shRNA) sequences in each of HS578T, MDA-MB-231 and SUM159PT claudin-low cell lines and followed this with Bulk-RNA sequencing. We present this comprehensive transcriptomic data set which provides a valuable resource for the analysis of NRP1-regulated signalling pathways in claudin-low breast cancer, paving the way for future studies of its potential as a targeted therapeutic.
Project description:Group 2 innate lymphoid cells (ILC2s) play critical roles in driving the pathogenesis of allergic airway inflammation. The mechanisms underlying the regulation of ILC2s remain to be fully understood. Here, we identified neuropilin-1 (Nrp1) as a surface marker of ILC2s in response to IL-33 stimulation. Nrp1 was abundantly expressed in ILC2s from lung under steady state, which was significantly reduced upon IL-33 stimulation. ILC2s with high expression of Nrp1 (Nrp1high) displayed lower response to IL-33, as compared with Nrp1low ILC2s. Transcriptional profiling and flow cytometric analysis showed that downregulation of AKT-mTOR signaling participated in the diminished functionality of Nrp1high ILC2s. These observations revealed a potential role of Nrp1 in ILC2s responses under allergic inflammatory condition.