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Altered bone marrow myelopoiesis contributes to kidney injury [ATAC-seq]

ABSTRACT: Altered bone marrow myelopoiesis contributes to kidney injury [ATAC-seq]

PROVIDER: PRJNA1162493 | ENA |

REPOSITORIES: ENA

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Altered bone marrow myelopoiesis contributes to kidney injury [scRNA-seq]

Project description:Altered bone marrow myelopoiesis contributes to kidney injury [scRNA-seq]

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Altered bone marrow myelopoiesis contributes to kidney injury [RNA-seq]

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Altered bone marrow myelopoiesis contributes to kidney injury [scRNA-seq]

Project description:The objectives of this study were to characterize bone marrow alteration in the context of kidney disease.

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Altered bone marrow myelopoiesis contributes to kidney injury [ATAC-seq]

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Gene expression data from myelomonocytes and whole kidney marrows in zebrafish adult kidney after deletion of miR-142-3p

Project description:hematopoiesis and myelopoiesis was tightly controled by microRNAs. In the zebrafish adult kidney, specific sets of genes were dysregulated in myelomonocytes or whole kidney marrow after deletion of miR-142-3p. microarrays were used to clarified the miR-142-3p regulatory network in myelopoiesis in miR-142-3p knockout zebrafish kidney and we identified distinct classes of up-regulated genes in zebrafish myelopoiesis or hematopoiesis after deletion of miR-142-3p. The myelomonocytes and whole kidney marrow (without erythrocytes) were sorted from wild-type or miR-142-3p double knockout zebrafish kidney at 60 dpf (four zebrafish kidneys and two independent repeats for each sample). Total RNA was extracted and hybridization on Affymetrix microarrays.

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Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in salt-sensitive hypertension

Project description:Although disturbed phosphate metabolism frequently accompanies chronic kidney disease, it is unclear whether it contributes to the progression of renal dysfunction. Here, we show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. Remarkably, four weeks of high salt loading resulted in a 2.5-fold increase in urinary phosphate excretion in Dahl salt-sensitive rats on a normal phosphorus diet. Inhibition of intestinal phosphate absorption using sucroferric oxyhydroxide (SF) in this model suppressed phosphaturia, attenuating glomerulosclerosis and tubulointerstitial injury without significantly affecting serum phosphate, blood pressure, or urinary sodium levels. In the kidney, macrophage infiltration and inflammatory cytokine induction were ameliorated by SF. Additionally, macrophage infiltration but not myofibril hypertrophy was alleviated in the heart. In vitro, phosphate loading to proximal tubule cells significantly increased inflammatory cytokine Ccl2, which was abolished by the removal of phosphate-containing nanoparticles but not by the knockdown of phosphate transporter Slc34a1. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with disturbed phosphate metabolism. These data demonstrate that increased phosphaturia promotes inflammation and renal injury from an early stage of salt-sensitive hypertension, and suggest the need for interventions against subclinical phosphate accumulation to improve the prognosis of hypertensive kidney disease.

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