Stabilin-1/CLEVER-1 is a multidomain protein present in lymphatic and vascular endothelial cells and in M2 immunosuppressive macrophages. Stabilin-1 functions in scavenging, endocytosis and leukocyte adhesion to and transmigration through the endothelial cells. We have analyzed the putative functions of Stabilin-1 in blood monocytes and found that in healthy individuals 60-80% of both CD14+CD16- and CD14+C16+ monocytes, but not CD14dimCD16+ monocytes, expressed Stabilin-1 on the surface. Microarray and RNAseq analysis was performed to get more insight into the effect of Stabilin-1 expression on human monocytes transcriptome. Overall design: The transcriptome of human monocytes transfected with Stabilin-1 siRNA was compared to that of control siRNA transfected monocytes
Monocyte Stabilin-1 Suppresses the Activation of Th1 Lymphocytes.
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View SamplesVascular adhesion protein-1 (VAP-1) is an endothelial cell-surface protein. It is also an enzyme posessing semicarbazide-sensitive amine oxidase activity (EC.1.4.3.6). VAP-1 is involved in leukocyte traffic. To study the role of VAP-1 in tumor immunity, we compared gene expression profiles in melanomas growing in VAP-1 -/- mice and their wid-type littermates.
Vascular adhesion protein-1 enhances tumor growth by supporting recruitment of Gr-1+CD11b+ myeloid cells into tumors.
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View SamplesStabilin-1/CLEVER-1 is a multidomain protein present in lymphatic and vascular endothelial cells and in M2 immunosuppressive macrophages. Stabilin-1 functions in scavenging, endocytosis and leukocyte adhesion to and transmigration through the endothelial cells. Overall design: The transcriptome of liver tissue in 2wk old and E17.5 Stab1 knock-out mice was compared to that of corresponding wild type mice
Enhanced Antibody Production in Clever-1/Stabilin-1-Deficient Mice.
Age, Specimen part, Subject
View SamplesThe distinction between lymphatic and blood vessels is biologically fundamental. Two immortalized cell lines, which have been widely used as models for endothelial cells of blood vascular origin, are the human microvascular endothelial cell line-1 (HMEC-1) and the telomerase-immortalized microvascular endothelial cell line (TIME). However, analysis of protein expression by flow cytometry revealed expression of lymphatic markers on these cell lines. Furthermore, functional in vitro leukocyte transmigration assays demonstrated deficiencies in several steps of the leukocyte extravasation cascade. Hence we performed this microarray analysis of the gene expression in HMEC-1 and TIME. We then compare the expression profiles to those of published blood- and lymphatic endothelial cells.
Plasticity of blood- and lymphatic endothelial cells and marker identification.
Cell line
View SamplesEscherichia coli (E. coli) amine oxidase (ECAO) encoded by tynA gene has been one of the model enzymes to study the mechanism of oxidative deamination of
Primary Amine Oxidase of Escherichia coli Is a Metabolic Enzyme that Can Use a Human Leukocyte Molecule as a Substrate.
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View SamplesStabilin-1/CLEVER-1 is a multidomain protein present in lymphatic and vascular endothelial cells and in M2 immunosuppressive macrophages. Stabilin-1 functions in scavenging, endocytosis and leukocyte adhesion to and transmigration through the endothelial cells. Overall design: The transcriptome of liver tissue in 5wk old Stab1 knock-out mice was compared to that of corresponding wild type mice
Stabilin-1 expression defines a subset of macrophages that mediate tissue homeostasis and prevent fibrosis in chronic liver injury.
Age, Specimen part, Subject
View SamplesThe neuronal ceroid lipofuscinoses (NCL) are a group of childhood inherited neurodegenerative disorders characterized by blindness, early dementia and pronounced cortical atrophy. The similar pathological and clinical profiles of different forms of NCL suggest that common disease mechanisms may be involved. Here, we have performed quantitative gene expression profiling of cortex from targeted knock out mice produced for Cln1 and Cln5 to explore NCL-associated molecular pathways. Combined microarray datasets from both mouse models exposed a common affected pathway: genes regulating cytoskeletal dynamics and neuronal growth cone stabilization display similar aberrations. We analyzed locus specific gene expression and showed regional clustering of Cln1 and three major genes of this pathway, further supporting a close functional relationship between the corresponding gene products, Cap1, Ptprf and Ptp4a2. The evidence from the gene expression data was substantiated by immunohistochemical staining data of Cln1-/- and Cln5-/- cortical neurons. These primary neurons displayed abnormalities in beta-tubulin and actin as well as abnormal intracellular distribution of growth cone associated proteins GAP-43, synapsin and Rab3. Our data provide the first evidence for a common molecular pathogenesis behind neuronal degeneration in CLN1 and CLN5. Since CLN1 and CLN5 code for proteins with distinct functional roles these data may have implications for other forms of NCL.
Brain gene expression profiles of Cln1 and Cln5 deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases.
Sex, Age, Specimen part, Disease
View SamplesBackground: Severe septic syndromes deeply impair innate and adaptive immunity. While neutrophils represent the first line of defense against infection, little is known about their phenotype and functions during sepsis-induced immunosuppression. The objective of this study was thus to perform for the first time a global evaluation of neutrophil alterations in immunosuppressed septic patients based on phenotypic, functional and transcriptomic studies. In addition, the potential association of these parameters and deleterious outcomes was assessed.
Marked alterations of neutrophil functions during sepsis-induced immunosuppression.
Disease
View SamplesMethylation of histone H3 lysine 4 (H3K4me) at actively expressed, cell type-specific genes is established during development by the Trithorax group of epigenetic regulators. In mammals, the Trithorax family includes KMT2A-D (MLL1-4), a family of SET domain proteins that function in large complexes to impart mono-, di-, and trimethylation at H3K4. Individual KMT2s and their co-factors are essential for embryonic development and the establishment of correct gene expression patterns, presumably by demarcating the active and accessible regions of the genome in a cell specific and heritable manner. Despite the importance of H3K4me marks in development, little is known about the importance of histone methylation in maintaining gene expression patterns in fully differentiated and non-dividing cell types. In this report, we utilized an inducible cardiac-specific Cre driver to delete the PTIP protein, a key component of a H3K4me complex, and ask whether this activity is still required to maintain the phenotype of terminally differentiated cardiomyocytes. Our results demonstrate that reducing the H3K4me3 marks is sufficient to alter gene expression patterns and significantly augment systolic heart function. These results clearly show that maintenance of H3K4me3 marks is necessary for the stability of the transcriptional program in differentiated cells. The array we performed allowed us to identify genes that are regulated by PTIP and histone methylation.
Loss of H3K4 methylation destabilizes gene expression patterns and physiological functions in adult murine cardiomyocytes.
Sex, Specimen part
View SamplesThis study is part of previous epidemiologic project, including a population-based survey (Sao Paulo Ageing & Health study (SPAH Study). The data from this study was collected between 2015 to 2016 and involved elderly women (ages ≥65 yeas) living in the Butanta district, Sao Paulo. The purpose of the study was identification of association between transcriptome and the osteo metabolism diseases phenotype, like osteoporosis, vertebral fracture and coronary calcification.
Overexpression of SNTG2, TRAF3IP2, and ITGA6 transcripts is associated with osteoporotic vertebral fracture in elderly women from community.
Sex, Age
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