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Bag3-P209L RNA Seq Project

ABSTRACT: Bag3-P209L RNA Seq Project

PROVIDER: PRJNA477769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7419540_1.fastq.gz	Fastqsanger.gz
	SRR7419540_2.fastq.gz	Fastqsanger.gz
	SRR7419550_1.fastq.gz	Fastqsanger.gz
	SRR7419550_2.fastq.gz	Fastqsanger.gz
	SRR7419541_1.fastq.gz	Fastqsanger.gz

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Bag3-P209L RNA Seq Project

Project description:Cardiac-specific Bag3-P209L transgenic (Tg+) mice develop dilated cardiomyopathy by 12 months of age. The goals of this project are to utilize RNA-sequencing to compare both cardiomyocyte and cardiac fibroblast transcriptomes between aged Bag3-P209L Tg+ and Bag3-WT mice to identify cardiomyocyte and fibroblast specific gene sets that contribute to the functional and morphological changes previously identified in Bag3-P209L Tg+ hearts.

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Cardiac fibroblast BAG3 regulates TGFBR2 signaling and fibrosis in dilated cardiomyopathy

Project description:Loss of Bcl2-associated anthanogene 3 (BAG3) is associated with dilated cardiomyopathy (DCM). Recent studies show that BAG3 regulates sarcomere protein turnover in cardiomyocytes (CMs). However, the function of BAG3 in other cell types of the heart is unknown. In this study, we used an isogenic pair of BAG3 knockout and wild-type human induced pluripotent stem cells (hiPSC) to interrogate the function of BAG3 in hiPSC-derived cardiac fibroblasts (CFs). Generating a series of conditional knockout (cKO) engineered heart tissues, we determined the contribution of CF BAG3 to engineered heart tissue function. Despite normal CM genotype, the loss of fibroblast-specific BAG3 (FBKO) caused a reduction in contractile force and an increase in cardiac fibrosis in the engineered heart tissues, recapitulating the phenotype of DCM. Using culture substrates with defined stiffness, we decoupled the mechanical activation of fibroblasts from their ligand response. In BAG3-/- CFs, we observed an increased sensitivity to transforming growth factor β (TGFβ) signaling and activation of a fibrogenic response when cultured at physiological stiffness (8kPa). Mechanistically, loss of BAG3 increased transforming growth factor receptor 2 (TGFBR2) levels. BAG3 binds TGFBR2 and mediates its ubiquitination and proteasomal degradation. To further validate these results, we performed single-nuclei sequencing of cardiac tissue from DCM patients carrying pathogenic BAG3 mutations. Mutations in BAG3 increased fibrotic gene expression in cardiac fibroblasts. Together, these results extend our understanding of the roles of BAG3 in heart disease beyond the cardiomyocyte-centric view. This study also highlights the ability of hiPSC-based models and tissue engineering to answer questions about the cell-type specific aspects of cardiac disease.

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Identification of genes involved in enhancement of hyperthermia sensitivity by knockdown of BAG3 in human oral squamous cell carcinoma cells

Project description:Hyperthermia (HT) treatments in combination with either chemotherapy, radiotherapy or both are used for patients with cancer in various organs. However, the acquisition of thermotolerance in cancer cells due to the increase in cytoprotective proteins attenuates the therapeutic effects of HT. BAG3 (BCL2-associated athanogene 3) is a cytoprotective protein that acts against various stresses including heat stress. Recently, we demonstrated that the inhibition of BAG3 improves cell death sensitivity to HT in cancer cells. However, a detailed molecular mechanism involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells is unclear. In this study, to identify genes involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells, global-scale gene expression analysis was carried out using a GeneChipÂ® system. Human oral squamous carcinoma cell HSC-3 cells were treated with a combination of HT (at 44Â°C for 90 min) and siRNA for BAG3 or luciferase. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was analyzed by an Affymetrix GeneChipÂ® system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerâs instructions.

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RNA-Seq Analysis

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