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RNA Sequencing of Cardiac in STZ-induced Rat model Uncovers Potential Target of Diabetic cardiomyopathy

ABSTRACT: RNA Sequencing of Cardiac in STZ-induced Rat model Uncovers Potential Target of Diabetic cardiomyopathy

PROVIDER: PRJNA813311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18249077_1.fastq.gz	Fastqsanger.gz
	SRR18249077_2.fastq.gz	Fastqsanger.gz
	SRR18249078_1.fastq.gz	Fastqsanger.gz
	SRR18249078_2.fastq.gz	Fastqsanger.gz
	SRR18249079_1.fastq.gz	Fastqsanger.gz

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RNA Sequencing of Cardiac in STZ-induced Rat model Uncovers Potential Target of Diabetic cardiomyopathy

Project description:Diabetic cardiomyopathy (DCM) is one of the major causes of heart failure in diabetic patients, but its pathogenesis remains unclear. Long non-coding RNAs (lncRNAs) are involved in the development of various cardiovascular diseases, but is little known in DCM. We build diabetic cardiomyopathy (DCM) rat model and investigated the genome-wide expression profiling of cardiac lncRNAs and mRNAs in rat model with and without DCM by RNA sequencing, to uncovers potential path mechanisms target of DCM.

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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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Role of micro-RNAs in pathophysiology of diabetic cardiomyopathy.

Project description:Diabetic cardiomyopathy (DCM), occurs independent of Hypertension, Coronary artery disease, or any other known cardiac disease and is characterized by myocardial fibrosis, myocytes loss and hypertrophy. The molecular mechanisms leading to these diseased cardiac phenotype are still being elucidated. A small number of studies have demonstrated that altered expression of several microRNAs are associated with ischemia , mechanical overload, or cardiovascular biology; however, much work is still required to identify individual or group of microRNAs and their role in the pathophysiology of diabetic cardiomyopathy. The aim of present study was to identify the expression of individual or group of microRNAs associated with myocytes hypertrophy and myocardial fibrosis during DCM. MicroRNAs expression profiles were studied in myocardium from High Fat diet and streptozotocin (STZ) induced diabetic (n=4) and non-diabetic (n=2) Wistar rats. All normalized and filtered microRNAs (n=780) processed for differential expression study using unpaired T-test in Gene spring in which unpaired comparison has been performed as test vs. control. After unpaired T-test, total 72 microRNAs were found to be significantly expressed with P-value ≤0.05. Differentially expression analysis was performed and at fold Change cut off ≥ 1.0, all 780 microRNA passed and 39 out of 780 microRNAs were differentially expressed on fold Change cut-off ≥1.5. These results indicate that during the development and progression of DCM, various microRNAs were differentially expressed and may participate in the regulation of various signaling pathways leading to myocytes hypertrophy, apoptosis and cardiac fibrosis.

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Project description:Diabetic cardiomyopathy is a major health problem world wide. CTRP9 is a secreted glycoprotein, which is mainly expressed in endothelial cells of the heart. In this study, we investigated the impact of CTRP9 on diabetic cardiomyopathy induced by high fat diet feeding. While the lack of CTRP9 in knock-out mice aggravated the disease, AAV9 mediated cardiac CTRP9 overexpression ameliorated diastolic cardiac dysfunction under these conditions. Mechanistically, we found that CTRP9 is required for insulin dependent cardiac glucose uptake and metabolism and that it counteracts cardiac inflammation.

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