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Spatially-patterned and functional kidney assembloids recapitulate progenitor self-assembly and enable high-fidelity in vivo disease modeling [hKPA_invivo_data]

ABSTRACT: The paired kidneys are the central organs of homeostasis for our body systems, the sophisticated structure and complex cells composition underpins kidneys’ functions. Here we reported the generation of human kidney progenitor assembloid (KPA) with expandable nephron progenitor cells (NPC) and ureteric bud (UB). These generated hSK showed patterned structure and included nephron, collecting duct and interstitium. More importantly, after transplantation hKPA developed more mature features and vasculature, and transplanted PKD2 hKPA developed abundant cysts, which shared some common features with human ADPKD kidney

ORGANISM(S): Homo sapiens

PROVIDER: GSE297772 | GEO | 2025/08/13

REPOSITORIES: GEO

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Spatially-patterned and functional kidney assembloids recapitulate progenitor self-assembly and enable high-fidelity in vivo disease modeling [hKPA_TT_data]

Project description:The paired kidneys are the central organs of homeostasis for our body systems, the sophisticated structure and complex cells composition underpins kidneys’ functions. Here we reported the generation of human kidney progenitor assembloid (KPA) with expandable nephron progenitor cells (NPC) and ureteric bud (UB). These generated hKPA showed patterned structure and included nephron, collecting duct and interstitium. More importantly, the application of TTNPB revealed the critical role of RA (retinoic acid) signaling pathway in hKPA generation.

2025-08-13 | GSE297771 | GEO

Spatially-patterned and functional kidney assembloids recapitulate progenitor self-assembly and enable high-fidelity in vivo disease modeling

2025-08-13 | GSE272707 | GEO

Spatially-patterned and functional kidney assembloids recapitulate progenitor self-assembly and enable high-fidelity in vivo disease modeling

Project description:The paired kidneys are the central organs of homeostasis for our body systems, the sophisticated structure and complex cells composition underpins kidneys’ functions. Here we report the generation of mouse kidney progenitor assembloid (mKPA) with expandable nephron progenitor cells (NPC) and ureteric bud (UB). Unexpectedly, versatile renal interstitial cells can be induced in kidney progenitor assembloid. Mechanistically, some NPC can be transdifferentiated into interstitial progenitor cells (IPCs) in KPA context, then induced IPCs differentiate into various renal interstitial cells. These kidney progenitors-based KPA highly resembled postnatal mouse kidneys with well pattern and showed essential renal physiological functions.

2025-08-13 | GSE262382 | GEO

Spatially-patterned and functional kidney assembloids recapitulate progenitor self-assembly and enable high-fidelity in vivo disease modeling

Project description:The paired kidneys are the central organs of homeostasis for our body systems, the sophisticated structure and complex cells composition underpins kidneys’ functions. Here we report the generation of mouse kidney progenitor assembloid (KPA) with expandable nephron progenitor cells (NPC) and ureteric bud (UB). Unexpectedly, versatile renal interstitial cells can be induced in kidney progenitor assembloids. Mechanistically, some NPC can be transdifferentiated into interstitial progenitor cells (IPCs) in KPA context, then induced IPCs differentiate into various renal interstitial cells. These kidney progenitors-based KPA highly resembled postnatal mouse kidneys with well pattern and showed essential renal physiological functions.

2025-08-13 | GSE264516 | GEO

Next Generation Sequencing of PKD2 mutant mice

Project description:Purpose: Determine the differential gene expression pattern between wildtype, Pkd2-KO and Pkd2-miR-214 KO mice Methods: kidney mRNA profiles of Pkd2-KO and Pkd2-mir-214-KO mice was sequenced with N of 3 in each group Results: 972 differentially expressed transcripts were identified between Pkd2-KO kidneys and Pkd2-miR-214-KO kidneys Conclusion: Deletion of miR-214 promotes interstitial inflammation in mouse models of ADPKD

2019-09-25 | GSE137945 | GEO

Repression of interstitial cell identity in nephron progenitor cells by Pax2 establishes the nephron-interstitium lineage boundary throughout mammalian kidney development

Project description:The kidney contains the functional units, the nephrons, surrounded by the renal interstitium. Previously, we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal interstitial progenitor cells form at the onset of kidney development, descendant cells from these populations contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, indicating a lineage boundary between the nephron and renal interstitial compartments. Currently, it is unclear how lineages are regulated during kidney organogenesis. We demonstrate that nephron progenitor cells lacking Pax2 activity failed to differentiate into nephron cells, but can switch fates into renal interstitium cell types. These data suggest that Pax2 function maintains nephron progenitor cells by repressing transdifferentiation into renal interstitial cell states. Thus, the lineage boundary between the nephron and renal interstitial compartments is maintained by the Pax2 activity in nephron progenitor cells during kidney organogenesis.

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Ontogeny of CD24 expression in the human fetal kidney

Project description:CD24, or heat stable antigen, is a cell surface sialoglycoprotein expressed on immature cells that disappears after the cells have reached their final differentiation stage. CD24 may be important in human embryonic kidney epithelial cell differentiation. In mice, CD24 expression is up-regulated in the early metanephros and localized to developing epithelial structures but the role and expression of CD24 in the developing human kidney has not been well described. In normal human fetal kidneys from 8 to 38 weeks gestation, CD24 expression was up-regulated and restricted to the early epithelial aggregates of the metanephric blastema and to the committed proliferating tubular epithelia of the S-shape nephron; however individual CD24+ cells were identified in the interstitium of later gestation and postnatal kidneys. In freshly isolated cells, FACS analysis demonstrated distinct CD24+ and CD24+133+ cell populations, constituting up to 16% and 14% respectively of the total cells analyzed. Isolated and expanded CD24+ clones displayed features of an epithelial progenitor cell line. Early fetal urinary tract obstruction resulted in an upregulation of CD24 expression, both in developing epithelial structures of early gestation kidneys and in the cells of the injured tubular epithelium of the later gestation kidneys. These results highlight the cell specific expression of CD24 in the developing human kidney and dysregulation in fetal urinary tract obstruction. We used microarrays to define the differences in global gene expression between obstructed and normal human fetal kidneys. We analyzed RNA extracted from human fetal kidneys between the gestational ages 8 and 18 weeks gestation. This dataset is part of the TransQST collection.

2009-11-11 | E-GEOD-18969 | biostudies-arrayexpress

Transcriptomic profile of Pdk2KO mice treated with RGLS4326

Project description:Kidney global mRNA expression profiles was carried out in the Pkd2-KO model following RGLS4326 treatment PBS-treated controls. We found that RGLS4326 treatment had a significant transcriptome-wide impact and globally de-repressed mRNAs of predicted miR-17 target genes in cystic kidneys of Pkd2-KO model

2019-08-08 | GSE134719 | GEO

Macrophage Accumulation and Cyst Expansion in Pkd2, Ift88, and Double Mutant Mouse Models

Project description:Kidney cyst formation occurs due to loss of cilia localized polycystin proteins (e.g., Pkd1 or Pkd2) or ciliary structure (e.g., Ift88 or Kif3a). However, cyst progression is more rapid in polycystin mutant mice compared to cilia mutant mice, and loss of cilia in the polycystin mutant background (e.g., Pkd2 and Kif3a mutation) greatly attenuates cyst development. This led to the proposal that the polycystins function to repress a cyst promoting pathway that is dependent on an intact cilium. Renal macrophages are also involved in regulating cyst progression, and the macrophage accumulation paralles with cyst expansion. but it is unknown whether this occurs through a cilia-dependent pathway or the consequence of cyst expansion. To address this question, we compared macrophage accumulation level and phenotypes in cystic kidneys from Pc2 mutant and Ift88; Pkd2 double mutant mice by prefromed 10x Genomics scRNAseq techniques. And to avoid the varying cyst severity in these mouse from different mutations, the cystic kidneys from Pc2 mutant and Ift88; Pkd2 double mutant mice were collected by adjusting for cystic indices rather than age.

2025-05-27 | GSE297737 | GEO

Epigenetic silencing of PKD1 in autosomal dominant polycystic kidney disease

Project description:ADPKD (Autosomal dominant polycystic kidney disease) is the most common inherited disorders and is characterized by growth of numerous cysts filled with fluid in the kidneys. Ultimately, it leads to kidney failure. The mutations of PKD1 and PKD2 account for approximately 85 and 15 percent of ADPKD, respectively. However, the mechanisms related to genetic mutation of PKD1 and PKD2 are still unclear. To investigate altered gene expression levels, Affymetrix microarray was performed using the kidney tissue from normal and ADPKD patients.

2012-02-16 | GSE35831 | GEO

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