Intestinal flora
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA743690 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Intestinal flora of rats Raw sequence reads
| PRJNA602787 | ENA
Project description:intestinal microflora in aged rats Raw sequence reads
| PRJNA789821 | ENA
Project description:Interventions: Four Groups:None
Primary outcome(s): Intestinal microflora
Study Design: Case-Control study
| 2676442 | ecrin-mdr-crc
Project description:They were the microbe in intestinal flora of mice in different treatment group. metagenome
| PRJNA306395 | ENA
Project description:This study delineated how small intestinal resident microflora impact gene expression in Paneth cells. Keywords: functional genomics; transcriptional profiling
2006-06-28 | GSE5156 | GEO
Project description:Defects in nephrogenesis can have detrimental effects on cardiovascular and renal health in adult life. This is confirmed by observations in the Munich Wistar Frömter (MWF) rat that exhibits a congenital nephron deficit and renal failure with age. We performed genome-wide transcriptome analysis in embryonic kidneys to identify candidate genes for the reduced nephron number in MWF. We compared MWF E15.5 with stage-matched spontaneously hypertensive rats (SHR) at E16. Microarray analysis revealed 311 transcripts representing 253 known genes with differential expression between MWF and SHR (FC >+1.5 or <-1.5, FDR<0.05).
2015-07-01 | GSE66079 | GEO
Project description:RATIONALE: Hypertension can lead to podocyte damage and subsequent apoptosis, eventually resulting in glomerulosclerosis. Although alleviating podocyte apoptosis has clinical significance for the treatment of hypertensive nephropathy, an effective therapeutic target has not yet been identified. The function of Septin4, a pro-apoptotic protein and an important marker of organ damage, is regulated by post-translational modification (PTM). However, the exact role of Septin4 in regulating podocyte apoptosis and its connection to hypertensive renal damage remains unclear. OBJECTIVE: We investigated the function and underlying mechanism of Septin4 in AngII-induced hypertensive nephropathy to discover a theoretical basis for targeted treatment. METHODS AND RESULTS: Using transgenic Septin4-K174Q mutant mice treated with the antioxidant Tempol, we found that hyperacetylation of the K174 site of Septin4 exacerbates AngII induced hypertensive renal injury resulting from oxidative stress. Proteomics and western blotting assays indicated that Septin4-K174Q activates the cleaved-PARP1-cleaved-Caspase3 pathway. In Septin4-knockdown human renal podocytes, Septin4-K174R, which mimics deacetylation at K174, rescues podocyte apoptosis induced by AngII. We conclude that Septin4, when activated through acetylation of K174 (K174Q), promotes hypertensive renal injury. Immunoprecipitation and mass spectrometry analyses identified SIRT2 as a deacetylase that interacts with the Septin4 GTPase domain and deacetylates Septin4-K174. In Sirt2-deficient mice and SIRT2-knockdown renal podocytes, Septin4-K174 remains hyperacetylated and exacerbates hypertensive renal injury. By contrast, in Rosa26-Sirt2-Flag (SIRT2-TG) mice and SIRT2-knockdown renal podocytes re-expressing wild-type SIRT2, Septin4-K174 is hypoacetylated and mitigates hypertensive renal injury. CONCLUSION: Septin4-K174R, which mimics deacetylation by SIRT2, inhibits the cleaved-PARP1-cleaved-Caspase3 pathway. Septin4-K174R acts as a renal protective factor, mitigating AngII-induced hypertensive renal injury. These findings indicate that Septin4-K174 is a potential therapeutic target for the treatment of hypertensive renal injury.
2022-12-05 | PXD038538 | iProX
Project description:Systemic hypertension has a profound impact on the renal vascular physiology. In order to elucidate the biological pathways and macromolecules deregulated by hypertension renal vessels were obtained by Laser Capture Microdissection (LCM) from Spontaneously Hypertensive Rats (SHR) and age-matched controls (20 weeks). Proteomic analysis was performed aiming to detect early molecular alterations associated with hypertension at the renal vessels before the onset of vascular damage. Proteomic analysis identified 688 proteins, of which 58 were differentially expressed (15 up-regulated and 43 down-regulated in SHR). Many of these proteins are involved in vascular tone regulation by modulating the activity of endothelial Nitric Oxide Synthase (eNOS) (e.g. Xaa-Pro aminopeptidase 1 (XPP1), N(G) N(G)-dimethylarginine dimethylaminohydrolase 1 (DDAH1), Dehydropteridine reductase (DHPR)) or in blood pressure control by regulating the renin-angiotensin system (e.g. Glutamyl aminopeptidase/Aminopeptidase A (AMPE), Aminopeptidase N (AMPN)). Moreover, pathway enrichment analysis revealed that the eNOS activation pathway is deregulated only in SHR. Our study demonstrates that hypertension causes early proteomic changes in the renal vessels of SHR. These changes are relevant to vascular tone regulation and consequently may be involved in the development of vascular damage and hypertensive nephrosclerosis. Therefore, the identified proteins could be considered as therapeutic targets.
2022-03-03 | PXD008792 | Pride
Project description:Development of renal transcriptome in spontaneously hypertensive rats (SHR) as compared to normotensive wistar kyoto rats (WKY) from birth to old age.
2008-04-30 | E-MEXP-1550 | biostudies-arrayexpress