Survey of Human Fetal Kidney Development Through Single Cell RNA Sequencing Analysis
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ABSTRACT:
PROVIDER: PRJNA431200 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6502980_1.fastq.gz | Fastqsanger.gz | |||
| SRR6502980_2.fastq.gz | Fastqsanger.gz | |||
| SRR6502990_1.fastq.gz | Fastqsanger.gz | |||
| SRR6502990_2.fastq.gz | Fastqsanger.gz | |||
| SRR6503000_1.fastq.gz | Fastqsanger.gz |
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Project description:Human kidney is a major metabolic organ, which plays a crucial role in regulating homeostasis of human body. However, gene expression characterizations of human fetal kidney development is still not fully explored. Here, we used single-cell RNA-seq to analyze more than 3,000 individual renal cells of human fetal kidneys covering over four months of development in vivo.We found co-expression of self-renewal and differentiation genes in cap mesenchyme, progenitors differed from that of mouse as they persistently express SIX1 throughout the renal morphogenesis. Besides, we recapitulated the transcription factors and signaling pathways potentially important for segmentation of nephron tubule. Furthermore, we explored the human specific features of the heterogeneous collecting duct epithelium. We also dissected the metabolism signatures of fetal kidney as well as the extracellular matrix composition of glomerulus mesangium. Eventually, we identified novel markers for renal tubules. Our study highlights the gene expression features of human fetal kidney development, which will contribute to dissecting the mechanisms of renal dysplasia and congenital nephrotic disease.
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Project description:Ketosis Induced Impairment of Fetal Kidney Development
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Project description:Little is known about the repertoire of nonhuman primate kidney genes expressed throughout development. The present work establishes an understanding of the primate renal transcriptome at different stages of fetal development and defines the framework of gene expression in the context of renal maturation, which provides a basis for identifying deviations in transcriptome expression resulting from suboptimal conditions during renal development. The baboon kidney transcriptome was characterized at 60 days gestation (DG), 90DG, 125DG, 160DG and adulthood (6-12 years) using human genome arrays to identify differential gene expression in the context of biological pathways and hierarchical clusters. Whole genome expression profiling showed 11,331 genes that were expressed during kidney development, 4,698 of which were differentially expressed among the developmental time points. Pathway analysis indicated activation of annotated pathways previously reported to be important to kidney development and pathways not reported as relevant to kidney development. QRT-PCR for genes central to these pathways validated expression profiles and revealed differences between males and females at specific times in gestation. Hierarchical clustering indicated that two clusters best fit the data, one containing genes that increased in expression from 60DG to adult and one that decreased. Cluster analysis also revealed gene splice variants with discordant expression profiles during development. For example, SMAD4, which is central to Wnt signaling, TGF-β signaling and cell cycle, showed up-regulation of the full-length splice variant during development and down-regulation of a shorter variant that is missing DNA binding and protein heterotrimerization domains suggesting decreased inhibition of cell proliferation, which may impact renal cell number and maturation. This study provides the first detailed genetic analysis of the developing primate kidney, and our findings of discordant expression of gene splice variants suggest that gene arrays likely provide a simplified view and demonstrate the need to study the fetal renal proteome.
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Project description:Maternal ketosis during pregnancy can impact fetal development, yet its effects on kidney development are not well understood. This study investigates the impact of maternal ketosis on offspring nephrogenesis using two mouse models: a ketogenic diet and β-hydroxybutyrate supplementation. Pregnant mice were subjected to either intervention from conception until birth. Offspring kidneys were analyzed at birth and in adulthood for nephron number, glomerular density, and renal function. Nephron progenitor cells (NPCs) were isolated from embryonic kidneys and analyzed using RNA sequencing, immunostaining, and quantitative PCR. Both ketosis models resulted in significantly reduced glomerular density at birth and a 25% decrease in nephron number in adult offspring, accompanied by impaired renal function. RNA sequencing revealed over 1,000 differentially expressed genes in the ketogenic diet group and 164 in the β-hydroxybutyrate group, with 67 overlapping genes. Pathway analysis showed downregulation of cell cycle and Myc target pathways, and upregulation of inflammatory pathways in both models. Immunostaining confirmed a 40% reduction in NPC proliferation and decreased c-Myc expression under ketotic conditions. Additionally, ketosis increased TNFα expression and activated the NFκB pathway in NPCs. These findings provide the first evidence linking maternal ketosis to impaired nephrogenesis, demonstrating a negative impact on offspring kidney development by altering NPC proliferation, Myc signaling, and inflammatory responses. This study highlights potential risks associated with ketogenic diets or other ketosis-inducing conditions during pregnancy.
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Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.
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Project description:Cytosine methylation is an epigenetic mark that dictates cell fate and response to stimuli. The timing and establishment of methylation logic during kidney development remains unknown. DNA methyltransferase 3a and 3b are the enzymes capable of establishing de novo methylation. We generated mice with genetic deletion of Dnmt3a and Dnmt3b in nephron progenitor cells (Six2Cre Dnmt3a/3b) and kidney tubule cells (KspCre Dnmt3a/3b). We characterized KspCre Dnmt3a/3b mice at baseline and after injury. Unbiased omics profiling, such as whole genome bisulfite sequencing, reduced representation bisulfite sequencing and RNA sequencing were performed on whole-kidney samples and isolated renal tubule cells. KspCre Dnmt3a/3b mice showed no obvious morphologic and functional alterations at baseline. Knockout animals exhibited increased resistance to cisplatin-induced kidney injury, but not to folic acid–induced fibrosis. Whole-genome bisulfite sequencing indicated that Dnmt3a and Dnmt3b play an important role in methylation of gene regulatory regions that act as fetal-specific enhancers in the developing kidney but are decommissioned in the mature kidney. Loss of Dnmt3a and Dnmt3b resulted in failure to silence developmental genes. We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci. Methylation patterns of kidneys from patients with CKD showed defects similar to those in mice with Dnmt3a and Dnmt3b deletion. Our results indicate a potential locus-specific convergence of genetic, epigenetic, and developmental elements in kidney disease development.
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