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Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [Bulk RNA-seq]

ABSTRACT: Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [Bulk RNA-seq]

PROVIDER: PRJNA1243446 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32904627_1.fastq.gz	Fastqsanger.gz
	SRR32904627_2.fastq.gz	Fastqsanger.gz
	SRR32904628_1.fastq.gz	Fastqsanger.gz
	SRR32904628_2.fastq.gz	Fastqsanger.gz
	SRR32904629_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells

Project description:Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells

| PRJNA1243443 | ENA

Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [scRNA-seq]

Project description:Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [scRNA-seq]

| PRJNA1243445 | ENA

Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [scRNA-seq]

Project description:Dysfunction of pancreatic alpha cells contributes to the pathophysiology of diabetes. Features of diabetic alpha cell dysfunction include glucagon hypersecretion, defects in proglucagon processing, and altered transcriptomic profile. The lack of an in vitro human alpha cell model has prevented the investigation, and potential correction, of these dysfunctional phenotypes. Here, we show that induction of endoplasmic reticulum stress in stem cell-derived alpha (SC-α) cells induces hypersecretion of glucagon. ER stress also increases the secretion of glicentin and expression of GLP-1, peptides produced by alternate cleavage of proglucagon by the prohormone convertase 1 (PC1/3) enzyme. Additionally, ER stress establishes a diabetic transcriptional state in SC-α cells characterized by downregulation of MAFB, as well as glycolysis and oxidative phosphorylation pathways. We show that sunitinib, a tyrosine kinase inhibitor, protects SC-α cells against the ER stress-induced glucagon hypersecretion phenotype. Thus, SC-α cell model can advance our knowledge of islets in health and diabetes.

2025-05-08 | GSE293265 | GEO

Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells [Bulk RNA-seq]

2025-05-08 | GSE293266 | GEO

Modeling Diabetic Endothelial Dysfunction with Patient-Specific Induced Pluripotent Stem Cells

Project description:Diabetes is a known risk factor for various cardiovascular complications, mediated by endothelial dysfunction. Despite the high prevalence of this metabolic disorder, there is a lack of in vitro models that recapitulate the complexity of genetic and environmental factors associated with diabetic endothelial dysfunction. Here, we utilized human induced pluripotent stem cell (iPSC)-derived endothelial cells (ECs) to develop in vitro models of diabetic endothelial dysfunction. We found that the diabetic phenotype was recapitulated in diabetic patient-derived iPSC-ECs, even in the absence of a diabetogenic environment. Subsequent exposure with culture conditions that mimic the diabetic clinical chemistry induced a diabetic phenotype in healthy iPSC-ECs but did not affect the already dysfunctional diabetic iPSC-ECs. RNA-seq analysis revealed extensive transcriptome-wide differences between cells derived from healthy individuals and diabetic patients. The in vitro disease models were used as a screening platform which identified angiotensin receptor blockers (ARBs) that improved endothelial function in vitro for each patient. In summary, we present in vitro models of diabetic endothelial dysfunction using iPSC technology, taking into account the complexity of genetic and environmental factors in the metabolic disorder. Our study provides novel insights into the pathophysiology of diabetic endothelial dysfunction and highlights the potential of iPSC-based models for drug discovery and personalized medicine.

2023-07-05 | GSE236430 | GEO

Modeling Diabetic Endothelial Dysfunction with Patient-Specific Induced Pluripotent Stem Cells

Project description:Modeling Diabetic Endothelial Dysfunction with Patient-Specific Induced Pluripotent Stem Cells

| PRJNA990795 | ENA

USP28 Serves as A Key Suppressor of Mitochondrial Morphofunctional Defects and Cardiac Dysfunction in the Diabetic Heart [RNA-seq]

Project description:The majority of diabetics are susceptible to cardiac dysfunction and heart failure, while conventional drug therapy cannot correct diabetic cardiomyopathy (DCM) progression. Herein, we assessed the potential role and therapeutic value of ubiquitin-specific protease 28 (USP28) on the metabolic vulnerability of DCM. cardiac USP28 deficient diabetic mice showed cardiac dysfunction, lipid accumulation, and mitochondrial disarrangement, compared to their controls. Conversely, USP28 overexpression improved systolic and diastolic dysfunction and ameliorated cardiac hypertrophy and fibrosis in the diabetic heart. Mechanistically, USP28 directly interacted with peroxisome proliferator-activated receptor α (PPARα), deubiquitinating and stabilizing PPARα (Lys152) to promote mitofusin 2 (Mfn2) transcription, thereby impeding mitochondrial morphofunctional defects.

2023-10-15 | GSE244904 | GEO

Atorvastatin Reduces Î²-Adrenergic Dysfunction in Rats with Diabetic Cardiomyopathy

Project description:Background: In the diabetic heart the Î²-adrenergic response is altered partly by down-regulation of the Î²1-adrenoceptor, reducing its positive inotropic effect and up-regulation of the Î²3-adrenoceptor, increasing its negative inotropic effect. Statins have clinical benefits on morbidity and mortality in diabetic patients which are attributed to âpleiotropicâ effects. The objective of our study was to investigate the role of statin treatment on Î²-adrenergic dysfunction in diabetic rat cardiomyocytes. Methods: Î²-adrenergic responses were investigated in vivo (echocardiography) and ex vivo (left ventricular papillary muscles) in healthy and streptozotocin-induced diabetic rats, who were pre-treated or not by oral atorvastatin over 15 days (50 mg.kg-1.day-1). Micro-array analysis and immunoblotting were performed in left ventricular homogenates. Data are presented as mean percentage of baseline Â± SD. Results: Atorvastatin restored the impaired positive inotropic effect of Î²-adrenergic stimulation in diabetic hearts compared with healthy hearts both in vivo and ex vivo but did not suppress the diastolic dysfunction of diabetes. Atorvastatin changed the RNA expression of 9 genes in the Î²-adrenergic pathway and corrected the protein expression of Î²1-adrenoceptor and Î²1/Î²3-adrenoceptor ratio, and multidrug resistance protein 4 (MRP4). Nitric oxide synthase (NOS) inhibition abolished the beneficial effects of atorvastatin on the Î²-adrenoceptor response. Conclusions: Atorvastatin restored the positive inotropic effect of the Î²-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by multiple modifications in expression of proteins in the Î²-adrenergic signaling pathway, particularly through the NOS pathway.

2017-06-27 | E-MTAB-5594 | biostudies-arrayexpress

Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-05-08 | GSE293267 | GEO

Pericyte-derived extracellular vesicle-mimetic nanovesicles ameliorates erectile dysfunction through Lipocalin 2 in the diabetic mice

Project description:Diabetes mellitus is one of the main causes of erectile dysfunction (ED). Due to neurovascular dysfunction, men with diabetic ED do not respond well to oral phosphodiesterase 5 inhibitors. Pericyte-derived extracellular vesicles-mimetic nanovesicles (PC-NVs) are known to play a role in promoting nerve regeneration in a mouse model of cavernous nerve injury. Here, we report that administration of PC-NVs can effectively promote penile angiogenesis and neural regeneration, thereby improving erectile function under diabetic conditions. We found that PC-NVs can induce endothelial proliferation, migration, and reduce cell apoptosis under diabetic conditions. In addition, PC-NVs induce neural regeneration in STZ-induced diabetic mice in vivo and ex vivo MPG or DRG explants under high-glucose conditions. We found that Lipocalin 2 (Lcn2) is a new target of PC-NVs in this process, indicating that PC-NVs exert their angiogenesis and nerve regeneration effects by activating MAP kinase, PI3K/Akt and suppressing P53 signaling pathway in an Lcn2-dependent manner under diabetic conditions. Our findings provide new conclusive evidence that PC-NVs mediate neurovascular regeneration and erectile function recovery under diabetic conditions through an Lcn2-dependent mechanism. Local administration of PC-NVs may be a promising treatment strategy for the treatment of diabetic ED.

2022-07-13 | GSE183220 | GEO

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