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Potential Antigens Involved In Delayed Xenograft Rejection in a GGTA1/CMAH DKO Pig-To-Monkey Model

ABSTRACT: When hyperacute rejection is avoided by deletion of Gal expression in the pig, delayed xenograft rejection (DXR) becomes a major immunologic barrier to successful xenotransplantation. This study was to investigate potential antigens involved in DXR. We isolated primary renal microvascular endothelial cells (RMEC) and aortic endothelial cells (AEC) from GGTA1/CMAH double-knockout (DKO) pig and immunized monkeys with both of these cells. After sensitization, monkey serum antibody binding and cytotoxicity to RMEC was significantlyhigher than to AEC,suggesting that RMEC are more immunogenic than AEC. Transcriptome sequencing of DKO pigs indicated that the expression of 1,500 genes was higher in RMEC than in AEC, while 896 genes was lower. The differentially-expressed genes were mainly related to cell and biological adhesion.

ORGANISM(S): Sus scrofa Homo sapiens Macaca fascicularis

PROVIDER: GSE99914 | GEO | 2019/07/07

REPOSITORIES: GEO

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Potential Antigens Involved In Delayed Xenograft Rejection in a GGTA1/CMAH DKO Pig-To-Monkey Model

Project description:Potential Antigens Involved In Delayed Xenograft Rejection in a GGTA1/CMAH DKO Pig-To-Monkey Model

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Gene expression profile in the cochlear tissue of Cmah-null mouse

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RNAseq analysis of bone marrow endothelial cells

Project description:Although endothelial cells (ECs) have been shown to contribute to HSC maintenance in bone marrow (BM), differential contributions of EC subtypes remain unknown, owing to the lack of methods to separate with high purity arterial (AEC) from sinusoidal (SEC) endothelial cells. We show that combination of podoplanin (PDPN) and Sca-1 expression distinguishes AEC from SEC where Sca1brightPDPN—CD45—Ter119— cells exhibit an arterial gene signature and PDPN+Sca1dimCD45—Ter119— marks sinusoids. PDPN can be substituted for antibodies against the adhesion molecules ICAM1 or E-selectin that also mark SEC. We performed functional analysis of these different types of endothelial cells and found that SCF secreated from AECs regulate HSCs.

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Gene expression profile of the Cmah gene depletion on mouse liver, lung, kidney and heart

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Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function Changes

Project description:We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. Further functional analysis demonstrated that GDM exposed cells have altered actin organization and barrier function. Our data indicate that exposure to GDM programs atypical morphology and barrier function in feto-placental endothelial cells by DNA methylation and gene expression change. The effects differ between AEC and VEC, indicating a stringent cell-specific sensitivity to adverse exposures associated with developmental programming in utero.

2018-08-01 | GSE103552 | GEO

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function

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Gene expression profile in the cochlear tissue of Cmah-null mouse

Project description:CMP-Neu5Ac hydroxylase (Cmah) disruption caused several abnormalities and diseases including hearing loss in old age. However, underling molecular mechanisms that give rise to age-related hearing loss (AHL) in Cmah-null mouse are still obscure. To identify differential gene expression profiles associated with Cmah disruption, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the cochlear tissues from a control mouse and a Cmah-null mouse. Total RNA was extracted and purified from the cochlear tissues of WT and Cmah-null mice using RNeasy columns (Qiagen; Valencia, CA, USA) according to the manufacturer’s protocol. The RNA quality was verified using an Agilent Bioanalyzer 2100 (Agilent Technologies; Palo Alto, CA, USA) using the RNA 6000 Pico Assay. Generation of double-stranded cDNA, preparation and labeling of cRNA, hybridization to Mouse Ref-8 v2.0 Expression BeadChip (Illumina, Inc.; San Diego, CA, USA), washing, and scanning were all performed according to the standard Illumina protocol. Arrays were scanned using the Illumina Bead Array Reader Confocal Scanner.

2015-07-10 | E-GEOD-70659 | biostudies-arrayexpress

Gene expression profile of the Cmah gene depletion on mouse liver, lung, kidney and heart

Project description:N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-specific genes whose function has been lost by disruption or deletion of the coding frame. It has been suggested that CMAH inactivation has resulted in biochemical or physiological characteristics that have resulted in human-specific diseases. To identify differential gene expression profiles associated with the loss of Neu5Gc expression, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the main tissues (liver, lung, kidney, and heart) from a control mouse and a Cmah-null mouse. Total RNA was extracted and purified from the liver, lung, kidney, and heart of WT and Cmah-null mice using RNeasy columns (Qiagen; Valencia, CA, USA) according to the manufacturer’s protocol. The RNA quality was verified using an Agilent Bioanalyzer 2100 (Agilent Technologies; Palo Alto, CA, USA) using the RNA 6000 Pico Assay. Generation of double-stranded cDNA, preparation and labeling of cRNA, hybridization to Mouse Ref-8 v2.0 Expression BeadChip (Illumina, Inc.; San Diego, CA, USA), washing, and scanning were all performed according to the standard Illumina protocol. Arrays were scanned using the Illumina Bead Array Reader Confocal Scanner.

2014-08-01 | E-GEOD-59964 | biostudies-arrayexpress

DNA methylation change involved in doxorubicin-induced testicular toxicity in mice

Project description:Testicular toxicity is one of the frequent adverse effects of cancer chemotherapy and the problem is that there is no effective biomarker. To find effective biomarkers, we focused on epigenetic mechanisms of male germline. Therefore, our study investigated the DNA methylation status of male germline under the testicular toxicity induced by doxorubicin(DXR), a widely used anticancer agent. We established mouse models of initial stage of testicular toxicity and testicular pre-toxicity by administrating 0.2 mg/kg and 0.02 mg/kg of DXR twice a week for 5 weeks. Western blotting analysis revealed the protein expression levels of DNA methyltransferases DNMT3a and DNMT3b were decreased in both the DXR administration groups. Consistently, comprehensive DNA methylation analysis of sperm DNA using MBD-seq revealed that the majority of methylation changes induced by DXR administration were hypomethylation. This study showed the possibility of early diagnosis of testicular toxicity by examining DNA methylation status of sperm.

2019-02-04 | GSE110227 | GEO

Array profiling of dystrophin-deficient mice with a secondary glycosylation defect

Project description:A deletion in the CMAH gene in humans occurred approximately 3.5 million years ago. This resulted in the inactivation of the CMP-Neu5Ac hydroxylase enzyme, and hence, in the specific deficiency in N-glycolylneuraminic acid (Neu5Gc), a form of sialic acid, in all modern humans. Although there is evidence that this molecular milestone in the origin of humans may have led to the evolution of human-specific pathogens, how deficiency in Neu5Gc might alter progression of non-infectious human diseases remains unanswered. Here, we have investigated cardiac and skeletal muscle gene expression changes in mdx mice, a model of Duchenne muscular dystrophy (DMD), that do or do not carry the human-like inactivating mutation in the mouse Cmah gene. We have evidence that Neu5Gc-deficiency in humans might explain some of the discrepancies in the disease phenotype between mdx mice and DMD patients. The study had four groups of mice: 1) Wild type, 2) Cmah KO (mice carrying a human-like mutation in the Cmah gene and hence have human-like deficiency in Neu5Gc sialic acid), 3) mdx (mouse model for Duchenne Muscular Dystrophy), and 4) mdx mice deficient in Cmah. Gene expression was studied in heart and gastrocnemius muscle samples. Three replicates per group/tissue.

2010-07-31 | E-GEOD-16438 | biostudies-arrayexpress

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