Project description:Wild type and CCR2-/- C57 mice were gavaged with carboxyl methyl cellulose (1%) or N-nitrosomethylbenzylamine(NMBA) 0.25 mg/kg body weight (BW) twice per week for 5 weeks. At the end of Week 25, the forestomach were harvested to carry out RNA resequencing. We found that CCR2 mediated monocyte infiltration promoted tumor evasion through activating PD-1 signaling pahtway.
Project description:Comparative analysis of FACS-sorted CCR2- and CCR2+ HSC in the steady state. CCR2+ HSC have fourfold higher proliferative rates than CCR2- HSC, are are biased towards the myeloid lineage and dominate the migratory HSC population. Comparison of pooled CCR2- and CCR2+ HSC (bone marrow from 20 mice pooled for each sample), three biological replicates each.
Project description:A number of inhibitors of chemokine CCL2 and its receptor CCR2 are in development and may find application for treating a range of inflammatory conditions, including autoimmune and viral arthritides. Herein we sought to determine the effect of CCR2 deficiency on arthritis caused by an arthritogenic alphavirus, Chikungunya virus. Chikungunya virus (LR2006-OPY1) was injected subcutaneously into the hind foot of either CCR2 knockout or wild-type control mice (n=4-6). At day 0 and d7 post infection, RNA from the feet was harvested, the RNA was pooled (4-6 feet per time point per mouse strain) and gene expression analysis was performed using Mouse Gene ST arrays (Affymetrix).
Project description:We microdissected discrete sub-regions of esophageal squamous cell carcinoma (ESCC) and analyzed the transcriptomes throughout three-dimensional (3D) tumor space.
Project description:A number of inhibitors of chemokine CCL2 and its receptor CCR2 are in development and may find application for treating a range of inflammatory conditions, including autoimmune and viral arthritides. Herein we sought to determine the effect of CCR2 deficiency on arthritis caused by an arthritogenic alphavirus, Chikungunya virus.
Project description:Purpose: To fully realize the potential molecular mechanism that S100A14 deficiency enhances esophageal carcinogenesis Methods: Total RNA of esophageal tumors in 4NQO WT and 4NQO S100A 14 CKO group mice was extracted with TRIzol Reagent. RNA libraries were constructed using an Illumina TruSeq RNA Sample Preparation kit according to the manufacturer’s protocol. A total of 150 base paired-end reads were sequenced using the Novaseq 6000 S4 platform. The read alignment was conducted using TopHat 2.0.13, and relative transcript abundances and differentially expressed genes were determined using the DESeq R package. Results: We identified 14,157 transcripts in esophageal tumors of 4NQO WT and 4NQO S100A14 CKO group mice. Approximately 8% of the transcripts showed differential expression between the esophageal tumors of 4NQO WT and 4NQO S100A 14 CKO group mice, with a fold change ≥1.0 and p value <0.05. Conclusions: Our study represents the first analysis of esophageal tumors derived from S100A14 CKO mice with biologic replicates, generated by RNA-seq.
Project description:We microdissected discrete sub-regions of esophageal squamous cell carcinoma (ESCC) and analyzed the transcriptomes throughout three-dimensional (3D) tumor space. Nine cases were used for TP/TC comparison, five cases were used for 3D analysis, one normal case was set as a control.
Project description:Comparative analysis of FACS-sorted CCR2- and CCR2+ HSC in the steady state. CCR2+ HSC have fourfold higher proliferative rates than CCR2- HSC, are are biased towards the myeloid lineage and dominate the migratory HSC population.
Project description:Monocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes are the most abundant subset in the blood. They express a CD14+CD16-CCR2+ phenotype, which confers on them the ability to migrate to inflammatory sites by quickly responding to CCL2 signaling. Here we identified and characterized the surge and expansion of a novel monocyte subset during SIV and HIV infection. They were undistinguishable from classical monocytes regarding CD14 and CD16 expression, but did not express surface CCR2. Transcriptome analysis of sorted cells confirmed that they represent a distinct subpopulation that expresses lower levels of inflammatory cytokines and activation markers than their CCR2+ counterparts. They exhibited impaired phagocytosis and deficient chemotaxis in response to CCL2 and CCL7, besides being refractory to SIV infection. We named these cells atypical CCR2- classical (ACC) monocytes, and believe they play an important role in AIDS pathogenesis, possibly reflecting an anti-inflammatory response against the extreme immune activation observed during SIV and HIV infection. Antiretroviral therapy caused this population to decline in both macaque and human subjects, suggesting that this atypical phenotype may be induced by viral replication. Expression profiling by NanoString nCounter gene expression system. Classical monocytes (CD14++CD16-) from six SIV-infected macaques (day 14 post inoculation) were sorted in two groups according to CCR2 expression.