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Tuning the 3D-microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease.

ABSTRACT: Tuning the 3D-microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease.

PROVIDER: PRJNA625948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11561626.fastq.gz	Fastqsanger.gz
	SRR11561627.fastq.gz	Fastqsanger.gz
	SRR11561628.fastq.gz	Fastqsanger.gz
	SRR11561629.fastq.gz	Fastqsanger.gz
	SRR11561630.fastq.gz	Fastqsanger.gz

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Tuning the 3D microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease

Project description:Tuning the 3D microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease

| PRJNA764927 | ENA

Tuning the 3D microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease

Project description:Embedding cells in 3D environments can enhance their physiological properties and tissue architecture can be controlled using bioprinting approaches. One cellular source for in vitro reconstituted kidney tubules are directly reprogrammed induced renal tubular epithelial cells (iRECs). Here, we investigated the compatibility of iRECs with different biomaterials as self assembly or bioprinting dependent guided growth approaches. We assess cell viability, morphology, their transcriptional changes and protein expression properties. iRECs showed high viability and biocompatibility with dispensing methods and bioinks. However, the morphology of multicellular aggregates was dramatically influenced by the microenvironment. Transcriptomic analyses revealed differentially expressed gene-signatures specific to each of the used biomaterials and to bioprinted tubule-like structures. In conclusion, we find that the 3D environment elicits a strong influence on the morphology and expression profiles of iRECs that unmasks disease phenotypes and can be harnessed for and tailored to experimental demands. Combining directly reprogrammed cells with the appropriate biomaterials will facilitate optimal construction of biomimetic kidney tubule and disease models at scale.

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Tuning the 3D-microenvironment of reprogrammed tubule cells enhances biomimetic modeling of polycystic kidney disease.

Project description:Mutations in PKD1 cause Autosomal Dominant Polycystic Kidney Disease (ADPKD). To further investigate the impact of Pkd1 knockout on renal tubular cells, a direct reprogramming approach was applied. After direct reprogramming of mouse embryonic fibroblasts to induced renal tubular epithelial cells (iRECs), Pkd1 knockout iREC clones were generated by Cre-mediated recombination of floxed Pkd1 alleles. The knockout clones were compared to their corresponding wild type clones by RNA Sequencing and transcriptome profiling.

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Dissection of Metabolic Reprogramming in Polycystic Kidney Disease Reveals Coordinated Rewiring of Bionergetic Pathways

Project description:Analysis of genome-wide transcriptional changes in cystic kidneys in the hypomorphic Pkd1V/V mouse model at postnatal day 10. The hypothesis tested in the present study was that metabolism is reprogrammed in polycystic kidney disease (PKD) in this model. Results provide important information of metabolic changes that affect glycolysis, mitochondrial metabolism, and fatty acid synthesis in the pathogenesis of PKD.

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Adamts1 Promotes Cyst Expansion in Polycystic Kidney Disease

Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by mutations in either the PKD1 or PKD2 genes leading to progressive cyst growth and often ESKD. We have previously demonstrated that with loss of Pkd1 the tubules can enlarge without an increase in tubular cell numbers, suggesting that tubular basement membrane remodeling is important for cystic dilation. Here we compared the transcriptomes from inducible tubule-specific knock out of Pkd1 (PkdTKO) and the uninduced littermate mice kidneys as controls. RNA sequencing revealed significant upregulation of 17 metalloproteinases. Of these, A Disintegrin and Metalloproteinase with Thrombospondin Motif 1 (Adamts1), expressed primarily by the proximal tubule, is the most significantly upregulated following loss of Pkd1 expression. Upregulation of Adamts1 in PkdTKO kidneys correlated with a significant increase in the 70 kDa cleavage product of the V1 isoform of versican, which localized to the tubule basement membrane (TBM) and adjacent interstitial mononuclear cells. Simultaneous deletion of both Adamts1 and Pkd1 (P/ATKO) reduced Adamts1 expression levels by >90%, prevented V1 versican cleavage, and reduced interstitial macrophage accumulation and activation. P/ATKO mice demonstrated slower cystic enlargement, improved BUN and creatinine and better survival than did PkdTKO mice. In conclusion, preventing Adamts1 upregulation following loss of tubular Pkd1 expression effectively reduced macrophage accumulation and TBM remodeling, slowing cyst growth and preserving renal function.

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