Long non-coding RNAs (lncRNAs) have emerged as critical regulators in cardiovascular diseases, particularly in the development and progression of cardiac hypertrophy. This thesis explores the role of the nuclear-enriched lncRNA NEAT1 in cardiac hypertrophy, focusing on its regulatory interaction with microRNA-22 (miR-22) and its influence on cardiomyocyte and gene expression. Using both in vivo mouse models of pressure overload-induced hypertrophy (transverse aortic constriction) and in vitro cellular assays, we examined how the absence or downregulation of NEAT1 affects cardiac remodeling. Bioinformatics analyses of differential gene expression were integrated with pathway enrichment tools (STRING and DAVID), while qPCR was used to validate changes in NEAT1 and miR-22 levels.
Long non-coding RNAs (lncRNAs) have emerged as critical regulators in cardiovascular diseases, particularly in the development and progression of cardiac hypertrophy. This thesis explores the role of the nuclear-enriched lncRNA NEAT1 in cardiac hypertrophy, focusing on its regulatory interaction with microRNA-22 (miR-22) and its influence on cardiomyocyte and gene expression. Using both in vivo mouse models of pressure overload-induced hypertrophy (transverse aortic constriction) and in vitro cellular assays, we examined how the absence or downregulation of NEAT1 affects cardiac remodeling. Bioinformatics analyses of differential gene expression were integrated with pathway enrichment tools (STRING and DAVID), while qPCR was used to validate changes in NEAT1 and miR-22 levels.
The Role of Long Non-Coding RNA NEAT1 In Cardiac Hypertrophy: A Potential Marker Perspective
SHAH MALEKPOUR, GHAZAL
2024/2025
Abstract
Long non-coding RNAs (lncRNAs) have emerged as critical regulators in cardiovascular diseases, particularly in the development and progression of cardiac hypertrophy. This thesis explores the role of the nuclear-enriched lncRNA NEAT1 in cardiac hypertrophy, focusing on its regulatory interaction with microRNA-22 (miR-22) and its influence on cardiomyocyte and gene expression. Using both in vivo mouse models of pressure overload-induced hypertrophy (transverse aortic constriction) and in vitro cellular assays, we examined how the absence or downregulation of NEAT1 affects cardiac remodeling. Bioinformatics analyses of differential gene expression were integrated with pathway enrichment tools (STRING and DAVID), while qPCR was used to validate changes in NEAT1 and miR-22 levels.| File | Dimensione | Formato | |
|---|---|---|---|
|
SHAH_MALEKPOUR_GHAZAL_.pdf
accesso aperto
Dimensione
2.06 MB
Formato
Adobe PDF
|
2.06 MB | Adobe PDF | Visualizza/Apri |
The text of this website © Università degli studi di Padova. Full Text are published under a non-exclusive license. Metadata are under a CC0 License
https://hdl.handle.net/20.500.12608/88745