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Functional targets of cilia dependent cyst activation (CDCA) and a potential therapeutic targets for treating polycystic kidney disease

ABSTRACT: functional targets of cilia dependent cyst activation (CDCA) and a potential therapeutic targets for treating polycystic kidney disease

PROVIDER: PRJNA972715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24565747_1.fastq.gz	Fastqsanger.gz
	SRR24565747_2.fastq.gz	Fastqsanger.gz
	SRR24565748_1.fastq.gz	Fastqsanger.gz
	SRR24565748_2.fastq.gz	Fastqsanger.gz
	SRR24565749_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

functional targets of cilia dependent cyst activation (CDCA) and a potential therapeutic targets for treating polycystic kidney disease

Project description:We applied unbiased cell type specific transcriptional profiling by translating ribosome affinity purification (TRAP) to mouse kidneys with polycystin-1 and cilia inactivation at a stage prior kidney tubule cyst formation. We identified differentially expressed actively translating mRNA that correlated with the cilia dependent cyst activation (CDCA) pattern common to male and female mice. This differential translatome offers opportunities for mechanistic discovery in polycystin and cilia related kidney phenotypes.

2024-02-23 | GSE232556 | 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

Transcriptional responses of CDCA treated Staphylococcus aureus cells

Project description:Analysis of Staphylococcus aureus treated by CDCA. Staphylococcus aureus cells are evaluated with RNA-seq to understand the genes affected by this antibacterial agent. Our results provide new vision on the mode of action by CDCA.

2022-10-15 | GSE193011 | GEO

To investigate the mechanisms of CDCA regulates proliferation of Porcine Small Intestinal Epithelial Cells (IPEC-J2)

Project description:The objective of this study was to investigate the effects of CDCA on the gene expression of IPEC-J2 cells. The control group (CON) treated with PBS and the CDCA group treated with both CDCA. Compared with the CON group, CDCA group could regulate the gene expression related proliferation genes.

2022-12-09 | GSE214153 | GEO

Transcriptomic Profiling of Polycystic Kidney Disease Identifies Paracrine Factors in the Early Cyst Microenvironment

Project description:Initial cysts that are formed upon Pkd1 loss in mice impose persistent stress on surrounding tissue and trigger a cystic snowball effect, in which local aberrant PKD-related signaling increases the likelihood of new cyst formation, ultimately leading to accelerated disease progression. Although many pathways have been associated with PKD progression, the knowledge of early changes near initial cysts is limited. To perform an unbiased analysis of transcriptomic alterations in the cyst microenvironment, microdomains were collected from kidney sections of iKsp-Pkd1del mice with scattered Pkd1-deletion using Laser Capture Microdissection. These microdomains were defined as F4/80-low cystic, representing early alterations in the cyst microenvironment, F4/80-high cystic, with more advanced alterations, or non-cystic. RNA sequencing and differential gene expression analysis revealed 953 and 8088 dysregulated genes in the F4/80-low and F4/80-high cyst microenvironment, respectively, when compared to non-cystic microdomains. In the early cyst microenvironment, several injury-repair, growth, and tissue remodeling-related pathways were activated, accompanied by mild metabolic changes. In the more advanced F4/80-high microdomains, these pathways were potentiated and the metabolism was highly dysregulated. Upstream regulator analysis revealed a series of paracrine factors with increased activity in the early cyst microenvironment, including TNFSF12 and OSM. In line with the upstream regulator analysis, TWEAK and Oncostatin-M promoted cell proliferation and inflammatory gene expression in renal epithelial cells and fibroblasts in vitro. Collectively, our data provide an overview of molecular alterations that specifically occur in the cyst microenvironment and identify paracrine factors that may mediate early and advanced alterations in the cyst microenvironment.

2023-12-27 | GSE231304 | GEO

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.

2024-09-30 | GSE270531 | GEO

Smoking is Associated with Shortened Airway Cilia

Project description:Background: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 μm airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers. Methodology/Principal Findings: Cilia length in normal nonsmokers and smokers was evaluated in aldehyde-fixed, paraffin-embedded endobronchial biopsies, and air-dried and hydrated samples brushed from human airway epithelium via fiberoptic bronchoscopy. In 28 endobronchial biopsies, healthy smoker cilia length was reduced 15% compared to nonsmokers (p<0.05). In 47 air-dried samples of airway epithelial cells, smoker cilia length was reduced 13% compared to nonsmokers (p<0.0001). Analysis of the length of individual, detached cilia in 17 samples, smoker cilia length was reduced 9% compared to nonsmokers (p<0.05). Finally, in 16 fully hydrated, unfixed samples, smoker cilia length was reduced 7% compared to nonsmokers (p<0.05). Conclusions/significance: Models predict that a reduction in cilia length would reduce mucociliary clearance, suggesting that smoking-associated shorter airway epithelial cilia plays a significant role in the pathogenesis of smoking-induced lung disease.

2012-12-13 | E-GEOD-16696 | biostudies-arrayexpress

MicroRNA profiling of human primary hepatocytes treated with CDCA, GW4064 or FGF19

Project description:We studied the effect of bile acid CDCA, FXR agonsit GW4064 and FGF19 on the expression levels of microRNA in cultured human primary hepatocytes

2010-04-20 | E-TABM-691 | biostudies-arrayexpress

Adamts1 Promotes Cyst Expansion in Polycystic Kidney Disease

Project description:Adamts1 Promotes Cyst Expansion in Polycystic Kidney Disease

| PRJNA1127459 | ENA

RNA-seq of human primary hepatocytes treated with FGF19 and CDCA

Project description:Primary human hepatocytes were treated with recombinant FGF19 (n=3), CDCA (n=3), endogenously produced FGF19 (n=3), or vehicle controls (n=3+3). Total RNA was harvested and sequenced with a strand-specific paired end RNA-seq protocol.

2021-02-13 | E-MTAB-8627 | biostudies-arrayexpress

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