Microbiome of Stone Monuments
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA610736 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Whole shotgun metagenomic sequencing from stool samples from calcium oxalate kidney stone formers and healthy control participants
| PRJEB39576 | ENA
Project description:Indian Historic Stone Ruins Metagenome
| PRJNA545121 | ENA
Project description:We recently reported elimination of renal crystals and migration of macrophages (Mφ) around crystals in hyperoxaluric mice, suggesting Mφs might eliminate crystals. Mφs are of 2 phenotypes: inflammatory (M1) and anti-inflammatory (M2). Because M2Mφs are considered to be involved in tissue repair and regeneration, we focused attention on their suppressive role in renal crystal formation. Hence, we investigated the gene array profiling of renal macrophages in stone model mice and CSF-1-deficient stone model mice.
2013-10-22 | GSE51466 | GEO
Project description:Kidney stone disease causes significant morbidity and increases health care utilization. In this dataset, we applied a single-nucleus assay to renal papila samples in order to charachterize the cellular and molecular niches in patients with calcium oxalate (CaOx) stone disease and healthy subjects. In addition to identifying cell types important in papillary physiology, we characterize collecting duct cell subtypes and an undifferentiated epithelial cell type that was more prevalent in stone patients. Despite the focal nature of mineral deposition in nephrolithiasis, we uncover a global injury signature characterized by immune activation, oxidative stress and extracellular matrix remodeling. We also identify the association of MMP7 and MMP9 expression with stone disease and mineral deposition, respectively. MMP7 and MMP9 are significantly increased in the urine of patients with CaOx stone disease, and their levels correlate with disease activity. Our results define the spatial molecular landscape and specific pathways contributing to stone-mediated injury in the human papilla and identify associated urinary biomarkers.
2023-05-04 | GSE231569 | GEO
Project description:We recently reported elimination of renal crystals and migration of macrophages (MM-OM-^F) around crystals in hyperoxaluric mice, suggesting MM-OM-^Fs might eliminate crystals. MM-OM-^Fs are of 2 phenotypes: inflammatory (M1) and anti-inflammatory (M2). Because M2MM-OM-^Fs are considered to be involved in tissue repair and regeneration, we focused attention on their suppressive role in renal crystal formation. Hence, we investigated the gene array profiling of renal macrophages in stone model mice and CSF-1-deficient stone model mice. B6C3Fe a/a-Csf1op/J wild type/homozygous mice were admistered 80mg/kg gyyoxylate (GOX) for 6days, then the kidneys were extracted and sorted CD11b+/CD11c+ macrophages using autoMACS. The gene expression of WT- and op/op-macrophages were investigated using bone marrow derived M1/M2 macrophages as controls.
2013-10-22 | E-GEOD-51466 | biostudies-arrayexpress
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development. Total RNA were extracted from kidneys of 12 newly born and 6 adult mice (half Aprt-/- and half control). Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips.
2010-01-13 | E-GEOD-18160 | biostudies-arrayexpress
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development.
2010-01-13 | GSE18160 | GEO