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SHROOM3 Deficiency aggravates Adriamycin-induced nephropathy accompanied by Focal Adhesion disassembly and stress fiber disorganization

ABSTRACT: SHROOM3 Deficiency aggravates Adriamycin-induced nephropathy accompanied by Focal Adhesion disassembly and stress fiber disorganization

PROVIDER: PRJNA1251520 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33156264_1.fastq.gz	Fastqsanger.gz
	SRR33156264_2.fastq.gz	Fastqsanger.gz
	SRR33156265_1.fastq.gz	Fastqsanger.gz
	SRR33156265_2.fastq.gz	Fastqsanger.gz
	SRR33156266_1.fastq.gz	Fastqsanger.gz

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SHROOM3 Deficiency aggravates Adriamycin-induced nephropathy accompanied by Focal Adhesion disassembly and stress fiber disorganization

Project description:This RNA-sequencing study investigates the role of SHROOM3 in podocyte function and its contribution to renal pathophysiology. Podocytes are highly specialized epithelial cells critical for glomerular filtration barrier integrity. The study explores how SHROOM3 deficiency affects podocyte cytoskeletal architecture and focal adhesion dynamics in the context of Adriamycin-induced nephropathy, a widely used experimental model of podocyte injury and proteinuric kidney disease. We performed transcriptome analysis using RNA-sequencing on human podocyte cell lines, comparing Control (n=4) and SHROOM3 knockdown (KD) podocytes (n=4). Our objective was to identify the molecular mechanisms and signaling pathways through which SHROOM3 regulates podocyte cytoskeletal organization, with particular focus on stress fiber formation and focal adhesion assembly/disassembly. The dataset provides comprehensive gene expression profiles revealing how SHROOM3 deficiency exacerbates podocyte injury, disrupts actin cytoskeleton dynamics, and impairs focal adhesion stability during nephropathy progression.

2025-04-17 | GSE294734 | GEO

Shroom3 Affects Neuroepithelial Morphogenesis through Regulating Cytoskeletal Proteins in Cynomolgus Monkey’s Organoids

Project description:The loss of SHROOM3 plays an important role at the neuroepithelial stage, demonstrating the indispensability of SHROOM3 and indicating the great potential of organoids in understanding the mechanism of neural tube defects (NTDs).

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Shroom3-Fyn interaction determines nephrin phosphorylation and Albuminuria in allografts

Project description:Glomerular RNA-sequencing: Shroom3 knockdown adult mice vs controls

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ARPE-19 adriamycin gene expression II

Project description:This study compared the gene expression change of ARPE-19 cells before and after adriamycin treatment

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Genome-wide association mapping for cardiomyocyte ploidy identifies Shroom3 as responsible for hyperpolyploidy and ventricular dilation

Project description:Cardiomyocyte (CM) polyploidization has been associated with cardiac injury responses, including regeneration and heart failure. However, our understanding of the comprehensive mechanisms governing CM ploidy and its influence on heart physiology has been hindered by a lack of experimental tools. To address this issue and uncover novel genetic regulators, we surveyed CM ploidy across a new genetic resource known as the Hybrid Rat Diversity Panel and find significant variation in ploidy phenotypes across the panel. Using select rat strains with divergent displays of CM ploidy, we found that hyperpolyploidization (≥8N) positively correlates with various physiological parameters namely left ventricular dilation and reduced ejection fraction. Genome-wide association mapping identifies several loci significantly associated with frequency of hyperpolyploid CMs. Investigation of genes harboring damaging protein coding variants identified enrichment of cytoarchitectural genes, of which the ACTIN-binding protein, Shroom3, was found to be strongly and specifically expressed in CMs and harbor 7 damaging protein coding variants. Indeed, CM-specific deletion of Shroom3 increased hyperpolyploidization in adult mice, while also promoting left ventricular dilation and reducing cardiac function. Furthermore, functional characterization of single nucleotide variants resulting in amino acid changes within SHROOM3 confirmed two protein coding variants that disrupted SHROOM3-ACTIN interaction. This study elucidates the genetic determinants of CM ploidy phenotypes and solidifies a relationship between CM ploidy and left ventricular function. Importantly, CM intrinsic expression of at least one gene mapped in this study, Shroom3, is confirmed to regulate CM hyperpolyploidization and cardiac function.

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Project description:The aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with adriamycin. To this end, a cDNA microarray was performed (Affymetrix’s Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to adriamycin treatment, and compared with matched tumor biopsy samples after completion of the adriamycin treatment schedule.

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Genome-wide association mapping for cardiomyocyte ploidy identifies Shroom3 as responsible for hyperpolyploidy and ventricular dilation [bulkRNA-Seq]

Project description:Cardiomyocyte (CM) polyploidy is widely observed across the animal kingdom and various ploidy states are associated with cardiac injury responses, including regeneration and heart failure. However, our understanding of the comprehensive mechanisms governing CM ploidy and its relationship with heart physiology has been hindered by a lack of experimental tools. To address this issue and uncover novel genetic regulators, we surveyed CM ploidy across a new genetic resource known as the Hybrid Rat Diversity Panel and founnd significant variation in ploidy phenotypes across the panel. Using select rat strains with divergent displays of CM ploidy, we found that hyperpolyploidization (≥8N) positively correlates with various physiological parameters namely left ventricular dilation and reduced ejection fraction. Genome-wide association mapping identified several loci significantly associated with frequency of hyperpolyploid CMs. Investigation of genes harboring damaging protein coding variants within these loci identified enrichment of cytoarchitectural genes, of which the ACTIN-binding protein, Shroom3, was found to be strongly and specifically expressed in CMs and harbors 7 damaging protein coding variants. CM-specific deletion of Shroom3 resulted in increased hyperpolyploidization and promoted left ventricular dilation and reduced ejection fraction. Furthermore, functional characterization of single nucleotide variants resulting in amino acid changes within SHROOM3 confirmed two protein coding variants that disrupted SHROOM3-ACTIN interaction and led to altered expression of cell cycle genes. This study elucidates the genetic determinants of CM ploidy phenotypes and solidifies a correlative relationship between CM ploidy and left ventricular function. Importantly, CM intrinsic expression of at least one gene mapped in this study, Shroom3, is confirmed to regulate CM hyperpolyploidization and cardiac function.

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Next Generation Sequencing of control (Untreated), PAN injured and Adriamycin injured human podocytes

Project description:Purpose: Next-generation sequencing (NGS) was used to identify cellular pathways and genes through systems-based analysis. The goals of this study are to identify NGS-derived transcriptome profiling (RNA-seq) in control (untreated) and Injured (PAN and Adriamycin) podocyte. These high throughput data were further validated through qRT–PCR methods to confirm the cellular pathways and genes affected due to the podocyte injury. Methods: Human podocytes were differentiated for 14 days by thermoswitching from 33⁰C to 37⁰C and removal of growth factors, insulin-transferrin-selenium from the medium. These podocytes were incubated 4hour in serum free RPMI medium and injury was induced by using PAN (100μg/ml) and Adriamycin (0.25μg/ml) treatment for 48 hours.Further, podocytes were processed for RNA isolation and submitted to Medical University of South Carolina Sequencing Core facility for RNA-Seq. All the experiments were performed in triplicates. Conclusions: Our study is first to describe the detailed analysis of PAN and Adriamycin induced podocyte transcriptomes using the RNA-seq technology. A comparative analysis of the differential expression profile was obtained between control vs PAN injured podocytes, and control vs Adriamycin injured podocytes. Complex genetic network and genes effected due to the injury will provide a platform to define biological pathways participate during podocytes injury process.

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RAD21-R450C variant is associated with corneal stroma disorganization

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