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Project description:Renal recovery following injury relies on cellular regeneration. In the mouse kidney following injury, injured epithelial cells undergoes de-differentiate, proliferate and re-differentiate into functional cells, following a a tightly controlled genetic programme where specific sets of genes are up-regulated. We used microarrays to detail the global programme of gene expression underlying cellular regeneration following injury with or without a HDAC inhibitor, m4PTB, treatment and identified distinct classes of up-regulated genes during this process. Male BALB/c mice underwent 26 minute unilateral ischemia-reperfusion (IR) with contralateral nephrectomy treated with vehicle or 100 mg/kg m4PTB 24 h after inducing renal injury, and kidneys harvested for RNA extraction 12 h later. We sought to obtain kidneys within a similar degree of injury in order to carefully evaluate the effect of m4PTB on expression profiles. To that end, we selected kidneys according to three different criteria of injury: (1) level of serum creatinine at Day1, (2) the level of blood urea nitrogen (BUN) (3) Kim1 expression by qPCR at Day1.5 using haevested kidneys
2013-03-01 | E-GEOD-42247 | biostudies-arrayexpress
Project description:NRK cells were exposed to serum-free, 10% FBS (control), 10% serum sampled from rats 24 hours after sham surgery (no kidney injury control), or 10% serum sampled from rats 24 hours after I/R AKI surgery (kidney injury serum). After 48 hours of exposure to serum, the NRK cells were harvested and processed for Agilent microarray We previously conducted a Phase I Clinical Trial in which Mesenchymal Stem/Stromal Cells (MSCs) were administered to patients at risk for developing acute kidney injury (AKI), and which suggested that MSC therapy is safe and effective in preventing both postoperative AKI and progression to CKD. It is well understood that AKI creates an internal environment that adversely affects not only the kidneys but also the function of distant organs and tissues. To study the consequences of the AKI environment on MSCs and renal cells, we developed an in vitro assay of exposing MSCs or cultured tubular cells (NRK Cells) to serum from animals that had AKI, or SHAM surgeries. Compared to SHAM sera, exposure of cells to AKI serum caused increased intra-cellular resazurin reduction, and activation of anti-oxidant genes,
2017-03-16 | GSE94678 | GEO
Project description:Delayed graft function (DGF) is commonly defined as dialysis in the first week post-transplant. This definition, though readily applicable, is too generic and unable to distinguish between “types� of DGF or time needed to recover function. We aimed to profile biological pathways in DCD kidney donors that correlate with DGF and discriminate different durations. N=30 DCD kidney biopsies were selected from the UK Quality in Organ Donation biobank and stratified according to DGF duration (immediate function, IF n=10; “short-DGF� (1-6 days), SDGF n=10; “long-DGF� (7-22 days), LDGF n=10). Samples were matched for donor and recipient demographics and analysed by label-free quantitative proteomics, yielding identification of N=3,378 proteins. Ingenuity Pathway Analysis on differentially abundant proteins showed that SDGF kidneys presented stress response pathways upregulation, while LDGF presented impaired response to stress, compared to IF. LDGF showed extensive metabolic deficits compared to IF and SDGF. DCD kidneys requiring dialysis only in the first week post-transplant present acute cellular injury at donation, alongside repair pathways upregulation. In contrast, DCD kidneys requiring dialysis longer beyond 7 days present minimal metabolic and antioxidant responses, suggesting current DGF definitions might not be adequate in distinguishing different types of injury in the donor kidneys contributing to DGF.
2024-05-23 | PXD038196 | Pride
Project description:Understanding kidney disease relies upon defining the complexity of cell types and states, their associated molecular profiles, and interactions within tissue neighborhoods. We applied multiple single-cell or -nucleus assays (>400,000 nuclei/cells) and spatial imaging technologies to a broad spectrum of healthy reference (45 donors) and diseased (48 patients) kidneys. This has provided a high resolution cellular atlas of 51 main cell types that include rare and novel cell populations. The multi-omic approach provides detailed transcriptomic profiles, epigenomic regulatory factors, and spatial localizations spanning the entire kidney. We further define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive or maladaptive repair, transitioning and degenerative states. Molecular signatures permitted localization of these states within injury neighborhoods using spatial transcriptomics, while large-scale 3D imaging analysis (~1.2 million neighborhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents the most comprehensive benchmark of cellular states, neighborhoods, outcome-associated signatures, and publicly available interactive visualizations.
2022-10-10 | GSE183277 | GEO
Project description:Understanding kidney disease relies upon defining the complexity of cell types and states, their associated molecular profiles, and interactions within tissue neighborhoods. We applied multiple single-cell or -nucleus assays (>400,000 nuclei/cells) and spatial imaging technologies to a broad spectrum of healthy reference (45 donors) and diseased (48 patients) kidneys. This has provided a high resolution cellular atlas of 51 main cell types that include rare and novel cell populations. The multi-omic approach provides detailed transcriptomic profiles, epigenomic regulatory factors, and spatial localizations spanning the entire kidney. We further define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive or maladaptive repair, transitioning and degenerative states. Molecular signatures permitted localization of these states within injury neighborhoods using spatial transcriptomics, while large-scale 3D imaging analysis (~1.2 million neighborhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents the most comprehensive benchmark of cellular states, neighborhoods, outcome-associated signatures, and publicly available interactive visualizations.
2022-10-10 | GSE183276 | GEO
Project description:8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest At t=0hr, mice had normal baseline renal function. At t=18hr, mice exhibited early renal injury, At t=42hr, mice had either recovered normal renal function or had persistent renal injury. We collected kidneys from 3 mice per time point. For the 42 hr time point, we collected kidneys from 3 mice with recovered renal function and kidneys from 3 mice with persistent renal injury. Mouse kidneys selected at successive stages of renal injury and recovery following systemic LPS challenge and volume resuscitation following LPS challenge.
2011-07-12 | E-GEOD-30576 | biostudies-arrayexpress
Project description:Understanding kidney disease relies upon defining the complexity of cell types and states, their associated molecular profiles, and interactions within tissue neighborhoods. We applied multiple single-cell or -nucleus assays (>400,000 nuclei/cells) and spatial imaging technologies to a broad spectrum of healthy reference (45 donors) and diseased (48 patients) kidneys. This has provided a high resolution cellular atlas of 51 main cell types that include rare and novel cell populations. The multi-omic approach provides detailed transcriptomic profiles, epigenomic regulatory factors, and spatial localizations spanning the entire kidney. We further define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive or maladaptive repair, transitioning and degenerative states. Molecular signatures permitted localization of these states within injury neighborhoods using spatial transcriptomics, while large-scale 3D imaging analysis (~1.2 million neighborhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents the most comprehensive benchmark of cellular states, neighborhoods, outcome-associated signatures, and publicly available interactive visualizations.
2022-10-10 | GSE183273 | GEO
Project description:Understanding kidney disease relies upon defining the complexity of cell types and states, their associated molecular profiles, and interactions within tissue neighborhoods. We applied multiple single-cell or -nucleus assays (>400,000 nuclei/cells) and spatial imaging technologies to a broad spectrum of healthy reference (45 donors) and diseased (48 patients) kidneys. This has provided a high resolution cellular atlas of 51 main cell types that include rare and novel cell populations. The multi-omic approach provides detailed transcriptomic profiles, epigenomic regulatory factors, and spatial localizations spanning the entire kidney. We further define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive or maladaptive repair, transitioning and degenerative states. Molecular signatures permitted localization of these states within injury neighborhoods using spatial transcriptomics, while large-scale 3D imaging analysis (~1.2 million neighborhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents the most comprehensive benchmark of cellular states, neighborhoods, outcome-associated signatures, and publicly available interactive visualizations.
2022-10-10 | GSE199711 | GEO
Project description:Understanding kidney disease relies upon defining the complexity of cell types and states, their associated molecular profiles, and interactions within tissue neighborhoods. We applied multiple single-cell or -nucleus assays (>400,000 nuclei/cells) and spatial imaging technologies to a broad spectrum of healthy reference (45 donors) and diseased (48 patients) kidneys. This has provided a high resolution cellular atlas of 51 main cell types that include rare and novel cell populations. The multi-omic approach provides detailed transcriptomic profiles, epigenomic regulatory factors, and spatial localizations spanning the entire kidney. We further define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive or maladaptive repair, transitioning and degenerative states. Molecular signatures permitted localization of these states within injury neighborhoods using spatial transcriptomics, while large-scale 3D imaging analysis (~1.2 million neighborhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents the most comprehensive benchmark of cellular states, neighborhoods, outcome-associated signatures, and publicly available interactive visualizations.
2022-10-10 | GSE183274 | GEO
Project description:8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest At t=0hr, mice had normal baseline renal function. At t=18hr, mice exhibited early renal injury, At t=42hr, mice had either recovered normal renal function or had persistent renal injury. We collected kidneys from 3 mice per time point. For the 42 hr time point, we collected kidneys from 3 mice with recovered renal function and kidneys from 3 mice with persistent renal injury.
2011-07-12 | GSE30576 | GEO