AC-ICAM: An Atlas and Compass of Immune-Colon-cancer-Microbiome interactions
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PROVIDER: PRJNA854256 | ENA |
REPOSITORIES: ENA
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Project description:AC-ICAM: An Atlas and Compass of Immune-Colon-cancer-Microbiome interactions
| PRJNA854255 | ENA
Project description:The bone marrow niche plays a critical role in controlling the fate of hematopoietic stem cells (HSCs) by integrating intrinsic and extrinsic signals. However, the molecular events in the HSC niche remain to be investigated. Here, we report that intercellular adhesion molecule-1 (ICAM-1) maintains HSC quiescence and repopulation capacity in the niche. ICAM-1-deficient mice (ICAM-1-/-) displayed significant expansion of phenotypic long-term HSCs with impaired quiescence, as well as favors myeloid cell expansion. ICAM-1-deficient HSCs presented normal reconstitution capacity during serial transplantation; however, reciprocal transplantation experiments showed that ICAM-1 deficiency in the niche impaired HSCs quiescence and repopulation capacity. In addition, ICAM-1 deletion caused failure to retain HSCs in the bone marrow and changed the expression profile of stroma cell-derived factors, possibly representing the mechanism for defective HSCs in ICAM-1-/- mice. Collectively, these observations identify ICAM-1 as a regulator in the bone marrow niche.
2018-06-21 | GSE114836 | GEO
Project description:The stimulation of trimethylation of histone H3 lysine 4 (H3K4) by H2B monoubiquitination (H2Bub) has been widely studied with multiple mechanisms proposed for this form of histone crosstalk. Cps35/Swd2 within COMPASS is considered to bridge these processes. However, a truncated form of Set1 (762-Set1) is reported to function in H3K4 trimethylation without interacting with Cps35/Swd2, and such crosstalk is attributed to the n-SET domain of Set1 and its interaction with the Cps40/Spp1 subunit of COMPASS. Here, we use biochemical, structural, in vivo, and ChIP-seq approaches to demonstrate that Cps40/Spp1 and the n-SET domain of Set1 are required for the stability of Set1 and not the crosstalk. Furthermore, the apparent wild-type levels of H3K4 trimethylation (H3K4me3) in the 762-Set1 strain is due to rogue methylase activity of this mutant resulting in the mislocalization of H3K4me3 from the promoter-proximal regions to gene bodies and intergenic regions. We have also performed detailed screens and identified yeast strains lacking H2Bub, but containing intact H2Bub enzymes, that have normal levels of H3K4me3, suggesting that ubiquitination may not directly stimulate COMPASS, but rather works in a context of the PAF and Rad6/Bre1 complexes. Our study demonstrates that the ubiquitination machinery and Cps35/Swd2 function to focus COMPASS’ H3K4me3 activity at promoter-proximal regions in a context dependent manner. ChIP-Seq for H3K4ME3 in S. cerevisie wild-type strains and strains expressing a truncated form of Set1: aa762-1080 Set1. H3K4ME3 ChIP-Seq was also compared for wild-type, leo1 knockout, and chd1 knockout strains
2014-01-09 | E-GEOD-53241 | biostudies-arrayexpress
Project description:To better understand the molecular effects of Enterotoxigenic Escherichia coli (ETEC) F4ab/ac infection, we performed a genome-wide comparison of the changes in DNA methylation in ETEC F4ab/ac infected porcine intestinal epithelial cells. Our data provides further insight into the epigenetic alterations of ETEC F4ab/ac infected porcine intestinal epithelial cells and may advance the identification of biomarkers and drug targets for predicting susceptibility to and controlling ETEC F4ab/ac induced diarrhea.
2020-04-06 | GSE143661 | GEO
Project description:In the present study, we aimed to determine the genes involved in inflammatory process of diabetic nephropathy. ICAM-1+/+ and ICAM-1-/- mice aged 8 weeks were divided into four groups: 1) nondiabetic ICAM-1+/+ mice (ND-WT), 2) nondiabetic ICAM-1-/- mice (ND-KO), 3) streptozotocin (STZ)-induced diabetic ICAM-1+/+ mice (DM-WT), and 4) STZ-induced diabetic ICAM-1-/- mice (DM-KO). Three months after the induction of diabetes, total RNA was extracted from each specimen of renal cortex. We examined gene expression profiles of four groups. We identified 193 genes; the ratio of expression level of DM-WT was >2 or <0.5 of that of DM-KO. Of 193 genes, hierarchical clustering identified 33 genes that were significantly upregulated only in DM-WT but not remarkable in ND-WT and ND-KO. Functional annotation of these 33 genes revealed that the significant functions of them were related to the immune or inflammatory process: immune response, response to stimulus, defense response, immune effector process and antigen processing and presentation. These genes contained several inflammatory related genes, such as chemokine (C-X-C motif) ligand 10, chemokine (c-c motif) ligand 12, and chemokine (c-c motif) ligand 8. In this cluster, we focused on cholecystokinin (CCK) because CCK is one of the most up-regulated genes. Real-time RT-PCR revealed that CCK mRNA expression was significantly up-regulated in DM-WT compared with DM-KO. These results suggest that CCK may play a critical role in the progression of diabetic nephropathy by controlling inflammation in diabetic kidney.
2014-10-08 | GSE21390 | GEO
Project description:TNF-a markedly induced the expression of IP-10 in NS-SV-AC cells. We identified TNF-a-induced genes in NS-SV-AC cells using Affymetrix GeneAtlasTM System.
2021-06-30 | GSE69050 | GEO
Project description:In the present study, we aimed to determine the genes involved in inflammatory process of diabetic nephropathy. ICAM-1+/+ and ICAM-1-/- mice aged 8 weeks were divided into four groups: 1) nondiabetic ICAM-1+/+ mice (ND-WT), 2) nondiabetic ICAM-1-/- mice (ND-KO), 3) streptozotocin (STZ)-induced diabetic ICAM-1+/+ mice (DM-WT), and 4) STZ-induced diabetic ICAM-1-/- mice (DM-KO). Three months after the induction of diabetes, total RNA was extracted from each specimen of renal cortex. We examined gene expression profiles of four groups. We identified 193 genes; the ratio of expression level of DM-WT was >2 or <0.5 of that of DM-KO. Of 193 genes, hierarchical clustering identified 33 genes that were significantly upregulated only in DM-WT but not remarkable in ND-WT and ND-KO. Functional annotation of these 33 genes revealed that the significant functions of them were related to the immune or inflammatory process: immune response, response to stimulus, defense response, immune effector process and antigen processing and presentation. These genes contained several inflammatory related genes, such as chemokine (C-X-C motif) ligand 10, chemokine (c-c motif) ligand 12, and chemokine (c-c motif) ligand 8. In this cluster, we focused on cholecystokinin (CCK) because CCK is one of the most up-regulated genes. Real-time RT-PCR revealed that CCK mRNA expression was significantly up-regulated in DM-WT compared with DM-KO. These results suggest that CCK may play a critical role in the progression of diabetic nephropathy by controlling inflammation in diabetic kidney. Male ICAM-1-/- mice (C57BL/6J background) were purchased from The Jackson Laboratory (Bar Harbor, ME). Male C57BL/6J mice (ICAM-1+/+) mice were used as controls. ICAM-1+/+ and ICAM-1-/- mice aged 8 weeks were divided into four groups (n = 5 each): 1) nondiabetic ICAM-1+/+ mice (ND-WT), 2) nondiabetic ICAM-1-/- mice (ND-KO), 3) streptozotocin (STZ)-induced diabetic ICAM-1+/+ mice (DM-WT), and 4) STZ-induced diabetic ICAM-1-/- mice (DM-KO). Mice in the diabetic groups received an intraperitoneal injection of STZ (Sigma Chemical, St.Louis, MO) at 200 mg/kg in citrate buffer (pH 4.5). Blood glucose levels were determined 7 days after STZ injection and only mice with blood glucose concentrations >16 mmol/L were used in the study. Nondiabetic ICAM-1+/+ and ICAM-1-/- mice received citrate buffer injections only. All mice had free access to standard diet and tap water. All animal procedures were performed according to the Guidelines for Animal Experiments at Okayama University Medical School, Japanese Government Animal Protection and Management Law (no. 105), and Japanese Government Notification on Feeding and Safekeeping of Animals (no. 6). Three months after the induction of diabetes, all mice were killed, and the kidneys were harvested. Total RNA was extracted from each specimen of renal cortex using standard protocol from RNeasy midi kit (Qiagen, Valencia, CA) at 3 months. The concentration and the quality of the total RNA sample were assessed by Agilent Bioanalyzer. Biotin-labeled target cRNA was prepared using First and Second strand cDNA Synthesis Kit (Amersham Biosciences, No. 320000) and In Vitro Transcription Kit (Amersham Biosciences, No.320001). Incubate total RNA (5 μg), diluted bacterial mRNA spike controls and T7 oligo (dT) primer for 10 min at 70 C. Add first-strand reaction components and incubate 1 hour at 42C. Add the first-strand cDNA product to the second-strand reaction components and incubate for 2 hours at 16 C. Double-strand cDNA was purified using QIAquick purification kit (Qiagen), eluted twice, each time with 30μl of nuclease-free water then dried in a SpeedVac concentrator. Prepare IVT mix of biotinylated UTP, ribonucleotides, and the 10x T7 enzyme mix and add to the resuspended cDNA. Incubate at 37C for 14 hours. Purify cRNA using RNeasy Mini Kit (Qiagen) and elute the cRNA twice, each time with 50 μl nuclease-free water. Measure the absorbance at 260 nm and 280 nm to determine the ratio (A260:A280=2). In 25 μl total volume, add 10 μg of cRNA to 5 μl of 5x fragmentation buffer and incubate at 94 C for 20 min. Bring 10 μg of fragmented cRNA, 78 μl of hybridization buffer component A, and 130 μl of hybridization buffer component B to a final volume of 260 μl with water. Incubate at 90C for 5 min and immediately chill on ice for 5 min. Slowly inject 250 μl of hybridization reaction mixture into array input port and seal ports with sealing strips. Set the shaker speed to 300 rpm and incubate slides for 18 hours at 37C in an Innove 4080 shaker. Remove the Flex Chamber using the hybridization removal tool. Then, place the bioarrays into the bioarray rack while it sits inside the medium reagent reservoir containing 0.75xTNT. Transfer the bioarray rack to the large reagent reservoir containing preheated 0.75xTNT, and incubate at 46 C for exactly 1 hour. Fill each slot of the small reagent reservoir with 3.4 ml of Cy5-Streptavidin working solution. Transfer the bioarray rack from the large reagent reservoir in to the small reagent reservoir and incubate bioarrays at RT for 30 min. Wash the bioarrays four times with 1xTNT at RT for 5 min. Rinse the bioarrays in 0.1xSSC/0.05%Tween by moving rack up and down 5 times in 5 seconds. Immediately follow the rinse with centrifugation to dry bioarrays, and store dried bioarrays in the dark. We scanned bioarrays with Axon GenePix 4000B and analyzed with CodeLink Expression Analysis software version 2.3.2. The 10,000 spot intensities on the scanned microarray image were normalized to a median value of 1 and data were exported for analysis with CodeLink Expression Analysis software version 2.3.2
2014-10-08 | E-GEOD-21390 | biostudies-arrayexpress
Project description:Atlas of the aging mouse colon
| PRJNA707433 | ENA