Single cell profiling reveals sex, lineage and regional diversity in adult mouse kidney
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA532850 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8895550.fastq.gz | Fastqsanger.gz | |||
| SRR8895541.fastq.gz | Fastqsanger.gz | |||
| SRR8895551.fastq.gz | Fastqsanger.gz | |||
| SRR8895542.fastq.gz | Fastqsanger.gz | |||
| SRR8895552.fastq.gz | Fastqsanger.gz |
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Project description:Renin expressing cells in the kidney’s juxta-glomeruluar compartment likely also serve as progenitors for adult glomerular cells in disease. Although these cells of renin lineage (CoRL) decrease in number with advancing kidney age, accompanied by less responsiveness to typical stimuli such as ACE-inhibition, mechanisms and the impact of sex as a biological variable with age are not known. Accordingly, labeled CoRL were sorted from individual young (2m) and aged (27m) male and female Ren1cCre|ZsGreen reporter mice, and their transcriptomic profiles analyzed by RNA seq. When both aged female and male mice were combined, there were 48 differentially expressed genes (DEG) compared to young mice. However, when compared to their young sex-matched mice, aged female and male mice had 159 and 503 DEGs respectively. In addition to marked differences in individual genes between aged female and male mice, gene ontology analysis showed major pathway differences by sex. The majority of DEGs in one sex did not significantly change or changed in the opposite direction in the other sex. These results show that in CoRL of advanced age, individual genes and gene ontologies change, but differ between female and male mice, highlighting sex related differences the aging process.
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Project description:Female sex protects against development of acute kidney injury (AKI). While sex hormones may be involved in protection, the role of differential gene expression is unknown. We conducted gene profiling in male and female mice with or without kidney ischemia-reperfusion injury. Mice underwent bilateral renal pedicle clamping (30 min), and tissues were collected 24 hours after reperfusion. RNA-sequencing was performed on proximal tubules and kidney endothelial cells. Female mice were resistant to ischemic injury compared to males, determined by plasma creatinine, histologic scores, neutrophil infiltration, and extent of apoptosis. Sham mice had sex-specific gene disparities in proximal tubule and endothelium, and male mice showed profound gene dysregulation with ischemia-reperfusion compared to females. After ischemia proximal tubules from females exhibited smaller increases compared to males in injury-associated genes Lcn2, Havcr1, and Krt18, and no upregulation of Sox9 or Krt20. Endothelial upregulation of adhesion molecules and cytokines/chemokines occurred in males, but not females. Upregulated genes in male ischemic proximal tubules were linked to tumor necrosis factor and Toll-like receptor pathways, while female ischemic proximal tubules showed upregulated genes in pathways related to transport. The data suggest that sex-specific gene expression profiles in male and female proximal tubule and endothelium may underlie disparities in susceptibility to AKI.
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Project description:Cardiac development arises from two sources of mesoderm progenitors, the first (FHF) and the second heart field (SHF). Mesp1 has been proposed to mark the most primitive multipotent cardiac progenitors common for both heart fields. Here, using clonal analysis of the earliest prospective cardiovascular progenitors in a temporally controlled manner during the early gastrulation, we found that Mesp1 progenitors consist of two temporally distinct pools of progenitors restricted to either the FHF or the SHF. FHF progenitors were unipotent, while SHF progenitors, were either uni- or bipotent. Microarray and single cell RT-PCR analysis of Mesp1 progenitors revealed the existence of molecularly distinct populations of Mesp1 progenitors, consistent with their lineage and regional contribution. Altogether, these results provide evidence that heart development arises from distinct populations of unipotent and bipotent cardiac progenitors that independently express Mesp1 at different time points during their specification, revealing that the regional segregation and lineage restriction of cardiac progenitors occurs very early during gastrulation. We used microarrays to characterize the molecular mechanisms that control Mesp1 progenitor specification and lineage segregation during the early stage of cardiac mesoderm formation,
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Project description:There is a clear sex bias in the incident rates and progressions of many kidney diseases and kidney cancers. To obtain a comprehensive understanding of the genetic and epigenetic regulation of kidney sexual dimorphism, we integrated single nucleus RNA and ATAC sequencing (snRNA-Seq and snATAC-Seq) and Visium spatial transcriptomics (ST) data to build a spatially resolved cell-type-specific molecular atlas for the mouse kidney throughout the lifespan, from embryo, newborn, youth, adolescence, adult to old age, of both sexes. We demonstrate that proximal tubules (PT) have the most sex-biased differentially expressed genes (DEGs) (164 and 227 for male and female respectively), which appear after 3 weeks of age and are associated with hormonal regulations. Notably, we reveal the potential mechanism of indirect and direct involvement of estrogen and androgen, respectively, in sex-biased gene expression regulations in the kidney. Specifically, regulon analysis shows that a set of female-biased DEGs, including Socs2, might be indirectly regulated by estrogen through prolactin-induced Jak2/Stat5 activation. On the other hand, chromatin accessibility investigation identifies androgen receptor motifs as significantly enriched in males, might be directly involved in regulating male-biased DEGs, such as Slco3a1, Serpinf2, Slc7a13, Slc22a30, Cyp4b1, and Acsm2. Sex-biased DEGs identified from mice, including several not previously highlighted, were validated by immunofluorescence and multiplex imaging data in human kidneys. Moreover, older male mice (92 weeks) display more aging-related gene alterations in loops of Henle and PTs, while older females have more aging-related gene alterations in fibroblasts. Our results provide the community with rich resources and better understanding of spatially resolved gene expression and hormone regulation for sexual dimorphism in the kidney across the lifespan.
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