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THADA deficiency improves glycemic control by promoting pancreatic β-cell function and survival under physiological and diabetic conditions

ABSTRACT: THADA deficiency improves glycemic control by promoting pancreatic β-cell function and survival under physiological and diabetic conditions

PROVIDER: PRJNA724995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14320952.fastq.gz	Fastqsanger.gz
	SRR14320953.fastq.gz	Fastqsanger.gz
	SRR14320954.fastq.gz	Fastqsanger.gz
	SRR14320955.fastq.gz	Fastqsanger.gz
	SRR14320956.fastq.gz	Fastqsanger.gz

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THADA deficiency improves glycemic control by promoting pancreatic β-cell function and survival under physiological and diabetic conditions

Project description:Purpose: The goals of this study are to explore the role of THADA in glucose homeostasis and insulin secretion Methods: Thada-activated beta-cell line was generated by CRISPR/dCas9-SAM system. Cells infected with dCas9 and non-targeting sgRNA lentiviruses were used as controls. Results: Transcriptomics analyses revealed that many genes were dys-regulated in beta-cells after THADA activation.

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Title Page Cardiac Gene Therapy Rescues Diabetic Cardiomyopathy and Lowers Blood Glucose

Project description:Diabetic cardiomyopathy, an increasingly global epidemic and a major cause of heart failure with preserved ejection fraction (HFpEF), is associated with hyperglycemia, insulin resistance, and intra-cardiomyocyte calcium mishandling. Here we identify that, in db/db mice with type 2 diabetes induced HFpEF, abnormal remodeling of cardiomyocyte transverse-tubule microdomains occurs with downregulation of the membrane scaffolding protein cardiac bridging integrator 1 (cBIN1). Transduction of cBIN1 by AAV9 gene therapy can restore transverse-tubule microdomains to normalize intracellular distribution of calcium handling proteins and, surprisingly, glucose transporter 4 (GLUT4). Cardiac proteomics revealed that AAV9-cBIN1 normalizes components of calcium handling and GLUT4 translocation machineries. Functional studies further identified that AAV9-cBIN1 normalizes insulin-dependent glucose uptake in diabetic cardiomyocytes. Phenotypically, AAV9-cBIN1 rescues cardiac lusitropy, improves exercise intolerance, and ameliorates hyperglycemia in diabetic mice. Restoration of transverse-tubule microdomains can improve cardiac function in the setting of diabetic cardiomyopathy, and also improve systemic glycemic control.

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Transcriptome profiling from adipose tissue during low-caloric diet reveals predictors of long-term weight and glycemic outcomes in obese, non-diabetic subjects

Project description:Background: Low-caloric diet (LCD) reduces fat mass excess, improves insulin sensitivity, and alters adipose tissue (AT) gene expression. Yet the relationship with long-term clinical outcomes remains unclear. Objective: We evaluated transcriptome alterations in AT during LCD and association with weight and glycemic outcomes both at LCD termination and 6-month after the LCD. Results: Upon LCD, we identified 1’173 genes differentially expressed; with 350 and 33 genes associated respectively with changes in BMI and Matsuda. Twenty-nine genes were associated with both endpoints. Pathway analyses highlighted enrichment in lipid and glucose metabolism. Models were constructed to predict weight maintainers. A model based on clinical baseline parameters could not achieve any prediction (validation’s AUC= 0.50 [0.36, 0.64]), while a model based on clinical changes during LCD yielded to good performance (AUC=0.73 [0.60, 0.87]). Incorporating baseline expression from the 18 genes outperformed the best clinical model (AUC=0.87 [0.77, 0.96], Delong’s p=0.012). Similar analyses were made to predict subjects with good glycemic improvements. Both baseline- and LCD-based clinical models yielded to similar performance (with best AUC=0.73 [0.60, 0.85]). Addition of expression changes during LCD improved substantially the performance (AUC=0.80 [0.69, 0.92], p=0.058). Conclusions: This study investigated AT transcriptome alterations following LCD in a large cohort of obese, non-diabetic patients. The identified genes enabled to significantly improve clinical models and predict long-term clinical outcomes. These biomarkers may help clinicians understanding the large inter-subject variability and better predict the success of dietary interventions.

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LncRNA/mRNA expression profiling for diabetic and reversal rat retina samples

Project description:We employed LncRNA/mRNA expression profiling as a discovery platform identify aberrantly expressed LncRNAs that fail to reverse back after hyperglycemia is terminated. Using rat model of diabetic retinopathy- metabolic memory, LncRNA array was performed in the retina of rats diabetic for eight months, or in poor glycemic control for four months followed by good glycemic control for four additional months. Expression of selected LncRNAs and their associated genes from these profiles were confirmed by quantitative real-time PCR.

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Project description:Severe angiopathy is a major driver for diabetes associated secondary complications. Knowledge on underlying mechanisms essential for advanced therapies to attenuate these pathologies is limited. Injection of ABCB5+ stromal precursors (SPs) at the edge of non-healing diabetic wounds in a murine db/db model, closely mirroring human type II diabetes, profoundly accelerates wound closure. Strikingly, enhanced angiogenesis was substantially enforced by the release of the ribonuclease angiogenin from ABCB5+ SPs. This compensates for the profoundly reduced angiogenin expression in non-treated murine and human chronic diabetic wounds. Silencing of angiogenin in ABCB5+ SPs prior to injection significantly reduced angiogenesis, reduced numbers of M2 macrophages and delayed wound closure in diabetic db/db mice implying an unprecedented key role for angiogenin in tissue regeneration in diabetes. These data hold significant promise for further refining SPs-based therapies of non-healing diabetic foot ulcers and other pathologies with impaired angiogenesis.

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Angiogenin Released from ABCB5+ Stromal Precursors Improves Healing of Diabetic Wounds by Promoting Angiogenesis

Project description:Angiogenin Released from ABCB5+ Stromal Precursors Improves Healing of Diabetic Wounds by Promoting Angiogenesis

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MicroRNA-148a-3p in pericyte-derived extracellular vesicles improves erectile function in diabetic mice by promoting cavernous neurovascular regeneration

Project description:Purpose: To investigate the regulatory role of microRNA (miR)-148a-3p in mouse corpus cavernous pericyte (MCPs)-derived extracellular vesicles (EVs) in the treatment of diabetes-induced erectile dysfunction (ED). Materials and Methods: Mouse corpus cavernous tissue was used for MCPs primary culture and EVs isolation. Small RNA sequencing analysis was performed to assess the type and content of miRs in MCPs-EVs. Four groups of mice were used: control nondiabetic mice and streptozotocin-induced diabetic mice receiving two intracavernous injections (days -3 and 0) of phosphate buffered saline, MCPs-EVs transfected with regent control, or MCPs-EVs transfected with miR-148a-3p inhibitor. The function of miR-148a-3p in MCPs-EVs was evaluated by tube formation assay, migration assay, TUNEL assay, intracavernous pressure, immunofluorescence staining, and western blot experiments. Results: We extracted EVs from MCPs and by small RNA sequencing analysis we found that miR-148a-3p is enriched in MCPs-EVs. Exogenous administration of MCPs-EVs can effectively promote mouse cavernous endothelial cell (MCECs) tube formation, migration, proliferation, and reduce MCECs apoptosis under high-glucose conditions. However, these effects are significantly attenuated in miR-148a-3p-depleted MCPs-EVs, which is extracted after inhibiting miR-148a-3p expression in MCPs. Repeated intracavernous injections of MCPs-EVs improves erectile function by inducing cavernous neurovascular regeneration in diabetic mice. Through online bioinformatics databases and luciferase report assays, we predict Pyruvate dehydrogenase kinase-4 (PDK4) is a potential target gene of miR-148a-3p. Conclusions: Our findings provide new and reliable evidence that miR-148a-3p in MCPs-EVs significantly enhances cavernous neurovascular regeneration by inhibiting PDK4 in diabetic mice.

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Metabolic Maturation Media Improves Physiological Function of Human iPSC-derived Cardiomyocytes

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Physiological hypoxia improves growth and functional differentiation of human intestinal epithelial organoids.

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Reduction of dietary glycemic load modifies expression of several miRNAs associated with energy balance and cancer pathways in premenopausal women

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