Project description:Stroke is a multiphasic progress characterized by neuron damage due to hypoxia followed by secondary damage from the subsequent inflammatory immune response. Infiltrating myeloid cells induce cerebral damage through pro-inflammatory cytokines, chemokines, proteases and generation of reactive oxygen species (ROS). Triggering receptor expressed on myeloid cells 1 (TREM1) is exclusively expressed on myeloid cells and acts as an amplifier of pro-inflammatory innate immune responses. Using microarray analysis, we aim to identify the expression differences and functional change of these myeloid cells after TREM1 knockout in mice post stroke.
Project description:To comprehensively characterize the impact of TREM1 deficiency specifically within the tumor myeloid populations, we selectively enriched the CD45+CD11b+ tumor-infiltrating myeloid cells from tumor-bearing Trem1+/+ and Trem1-/- mice for scRNA-seq analysis.
Project description:To gain a global understanding of the impact of TREM1 silencing, we analyzed the CD45+ tumor infiltrating cells (TICs) of B16F10 tumor-bearing Trem1+/+ and Trem1-/- mice. Utilizing the 10x Genomics Chromium Platform, we analyzed approximately 5390 cells per sample with a coverage rate of 15493 genes per cell.
Project description:To evaluate the change of gene expression at cerebral infarction by the treatment of IV-human umblical cord derived mesenchymal stem cell. RNA was isolated from the ipsilateral hemisphere to MCAo in rats. At 72 h post-MCAo, the ipsilateral hemisphere subjected to MCAo was used for mRNA microarray. RNA was isolated from the ipsilateral hemisphere to MCAo in rats without MCAo (control group, n=5), rats treated with 1x106 IV-hUMSC (hUMSC group, n=6) and saline (saline group, n=5) at 24h post-MCAo.
Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study. Total RNA isolated from sham, MCAo and MCAo+nPLA rat brains, was pooled to minimize inter-individual variation and hybridized to each array of the RAE-230A or U34A GeneChipTM according to protocols described in the GeneChipTM expression analysis package (Affymetrix, CA).
Project description:To investigate the function of TREM1 in the regulation of innate immune cell metabolism, we established mice in which TREM1 target gene has been genetically deleted. We then performed gene expression profiling analysis using data obtained from RNA-seq of 500,000 different cells from young and old WT and TREM1-/-mice.
Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study.
Project description:In this study we showed that Trem1 is one of genes that were differentially regulated in donor monocytes recovered from non-inflamed and inflamed small intestine of recipient mice. We, therefore, aimed at investigating the role of Trem1 on regulating the monocyte adapatation and differentiation in a context-dependent manner. Thus, the gene expression of WT and Trem1-deficient donor monocytes that are recruited to non-inflamed and inflamed small intestine one day after transfer.
Project description:To investigate the function of TREM1 in the regulation of innate immune cell function, we established mice in which TREM1 target gene has been genetically deleted. We then performed gene expression profiling analysis using data obtained from RNA-seq of microglia from young and old WT and TREM1-/-mice and from 5XFAD and 5XFADxTREM1+/- mice