MRNA-seq analysis of RAGE knock-in (RageAHA/AHA) and RAGE-/- mice
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PROVIDER: PRJNA728682 | ENA |
REPOSITORIES: ENA
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Project description:Cell surface heparan sulfate (HS) plays an essential role in RAGE signaling by inducing RAGE oligomerization. To understand the physiological significance of HS-induced RAGE oligomerization in vivo, we generated RAGE knock-in mice (RageAHA/AHA) by introducing point mutations to specifically disrupt HS–RAGE interaction. The RAGE variant expressed by RageAHA/AHA mice demonstrated normal ligand-binding but greatly impaired capacity of HS-binding and oligomerization. To grasp the full scale of the alteration in gene expression caused by knocking out Rage, we performed a RNAseq analysis of mature neutrophils and lung from WT, RageAHA/AHA and Rage-/- mice. The overall number of differently regulated genes (DEGs) in Rage-/- neutrophils were almost 2.5 times higher than in RageAHA/AHA neutrophils (603 vs. 247). In contrast, the number of DEGs were much less in lungs compared to neutrophils in both strains (202 DEGs in Rage-/- lungs and merely 31 DEGs in RageAHA/AHA lungs), however the difference between the two genotypes was even more dramatic in lungs (7-fold) than we observed in neutrophils (2.5-fold). By comparing transcriptomes of neutrophils and lung tissues from RageAHA/AHA and Rage-/- mice, we present clear evidence that complete deficiency of RAGE had much broader impact on global gene expression compared to point mutations of RAGE.
2021-05-11 | GSE174178 | GEO
Project description:To further characterize differential expression of miRNA and mRNA levels in livers of 12 weeks old male Tax1BP1 wildtype and knock-out mice, the untreated mice were sacrificed and miRNA and mRNA levels were determined
2020-10-06 | GSE98908 | GEO
Project description:Differential expression of miRNA and mRNA in Tax1BP1 knock-out mice
| PRJNA386865 | ENA
Project description:Objective – Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function. Research Design and Methods – We bred OVE26 mice with homozygous RAGE knock out (RKO) mice and examined structural changes associated with DN and used inulin clearance studies and albumin:creatinine measurements to assess renal function. Affymetrix Mouse 430.2 microarrays were used to measure the differential expression of OVE26vsFVB(WT) mice. Transcriptional changes in the TGF-?1 and Plasminogen activator inhibitor 1 gene products were measured by pcr to investigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice. Results - Deletion of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte effacement, and albuminuria. The significant 29% reduction in glomerular filtration rate observed in OVE26 mice was completely prevented by deletion of RAGE. Increased transcription of the genes for Plasminogen activator inhibitor 1, TGF-?1, TGF-? induced, ?1- (IV) collagen observed in OVE26 renal cortex significantly reduced in OVE26 RKO kidney cortex. ROCK1 activity was significantly lower in OVE26 RKO compared to OVE26 kidney cortex. Conclusions - These data provide compelling evidence for critical roles for RAGE in the pathogenesis of DN and suggest that strategies targeting RAGE in long-term diabetes may prevent loss of renal function. The differential gene expression of OVE26 (diabetics) vs FVB (nodiabetic WT) mice was measured using Affymetrix Mouse 430.2 arrays.
2011-02-22 | E-GEOD-20844 | biostudies-arrayexpress
Project description:We seprated the primodial germ cells using MACS from E12.5 stages in WT and Rif1-knock out mice, and using modified Smart-seq2 methods to get 1,000 cells library.
2024-03-21 | GSE169495 | GEO
Project description:Purpose: The goal of this study is to identify genes and molecular pathways whose expression is altered in the livers of Gpr151 knock-out (KO) mice compared to Gpr151 wild-type (WT). Methods: Total RNA was isolated from livers of fasted (5h) 16-week-old male mice. Deep sequencing of RNA from three wild-type and three knock-out mice was done using the mRNA-Seq pipeline at Novogene. The sequence reads that passed quality filters were aligned to the mouse GRCm38.p6 genome using STAR 2.6.1d. Differential expression testing was conducted using DESeq2. Results: Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the mouse genome (build mm10) and identified 54,532 transcripts in the livers of Gpr151 WT and KO mice. RNA-seq data identified 79 transcripts which were significantly upregulated in KO (p-adj < 0.05, log2FoldChange>1) and 338 transcripts which were significantly downregulated (p-adj<0.05, log2FoldChange<-1) in KO. Conclusions: Our study represents the first detailed analysis of the liver transcriptome of Gpr151 KO mice.
2022-10-14 | GSE196535 | GEO
Project description:Objective – Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function. Research Design and Methods – We bred OVE26 mice with homozygous RAGE knock out (RKO) mice and examined structural changes associated with DN and used inulin clearance studies and albumin:creatinine measurements to assess renal function. Affymetrix Mouse 430.2 microarrays were used to measure the differential expression of OVE26vsFVB(WT) mice. Transcriptional changes in the TGF-β1 and Plasminogen activator inhibitor 1 gene products were measured by pcr to investigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice. Results - Deletion of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte effacement, and albuminuria. The significant 29% reduction in glomerular filtration rate observed in OVE26 mice was completely prevented by deletion of RAGE. Increased transcription of the genes for Plasminogen activator inhibitor 1, TGF-β1, TGF-β induced, α1- (IV) collagen observed in OVE26 renal cortex significantly reduced in OVE26 RKO kidney cortex. ROCK1 activity was significantly lower in OVE26 RKO compared to OVE26 kidney cortex. Conclusions - These data provide compelling evidence for critical roles for RAGE in the pathogenesis of DN and suggest that strategies targeting RAGE in long-term diabetes may prevent loss of renal function.
2011-02-22 | GSE20844 | GEO
Project description:SCA17 knock-in mice brain transcriptomes
| PRJNA605839 | ENA
Project description:Hyperoxia in FGF10 knock-down mice
| PRJNA306852 | ENA
Project description:Purpose: The goals of this study are to compare NGS-derived skin transcriptome profiling (RNA-seq) in wild type mice with TTP delta ARE knock-in mutants. Methods: Skin mRNA profiles of approximately 27 week old wild-type (WT) and TTP delta ARE knock-in mice were generated by deep sequencing, with five biological replicates, using Illumina sequencers. The skin RNA samples were prepared from skin biopsies from treated but not papillomatous skin from mice treated with a standard DMBA-TPA protocol for 20 weeks. The sequence reads that passed quality filters were mapped to mm10 with STAR Aligner followed by featureCounts and DESeq2 anlysis. Results: We observed 1144 statistically differentially expressed genes (232 and 912 up- and down-regulated genes in TTP delta ARE mice, respectively, with fold changes >2 and FDR<0.05. Conclusions: Regulated overexpression of TTP by a stablizing deletion in the 3'UTR of its mRNA causes many changes in gene expression in mice subjected to a standard skin papilloma protocol.
2021-04-13 | GSE148199 | GEO