EXPRESSION OF CARDIOMIRS BY ADENO-ASSOCIATED VECTORS AND FUNCTIONALISED NANOPARTICLES FOR THE TREATMENT OF MYOCARDIAL INFARCTION (Q3161197): Difference between revisions
Jump to navigation
Jump to search
(Removed claim: summary (P836): The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic po...) |
(Created claim: summary (P836): The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic poss...) |
||||||||||||||
| Property / summary | |||||||||||||||
The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic possibilities for the treatment of IM, based on the application of gene therapy and nanotechnology. First, the therapeutic role of microRNAs in the suppression of fibrosis (miR-29b and miR-133a) and in the protection (miR-133a and miR-199a) and proliferation (miR-199a) of cardiomyocytes will be studied. For this purpose, these microRNAs will be overexpressed in vivo, using cardiotropic adenoassociated viral vectors (AAVs), built with specific promoters of cardiomyocytes or fibroblasts and adjustable by tetracycline. In addition, an alternative method for sustained microRNA expression based on the use of biocompatible and biodegradable PLGA-PEG nanoparticles (NPs) and functionalised with the RGD peptide will be evaluated. The dose and therapeutic effect of VPAs-miR and NPs-miR shall be determined in an acute murine model of IM. The possible functional improvement will be analysed by echocardiography and its proper remodeling by histological analysis. This project has been designed to evaluate a novel therapy for the treatment of IM, based on the over-expression of therapeutic miRNAs through the application of gene therapy and nanotechnology. (English) | |||||||||||||||
| Property / summary: The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic possibilities for the treatment of IM, based on the application of gene therapy and nanotechnology. First, the therapeutic role of microRNAs in the suppression of fibrosis (miR-29b and miR-133a) and in the protection (miR-133a and miR-199a) and proliferation (miR-199a) of cardiomyocytes will be studied. For this purpose, these microRNAs will be overexpressed in vivo, using cardiotropic adenoassociated viral vectors (AAVs), built with specific promoters of cardiomyocytes or fibroblasts and adjustable by tetracycline. In addition, an alternative method for sustained microRNA expression based on the use of biocompatible and biodegradable PLGA-PEG nanoparticles (NPs) and functionalised with the RGD peptide will be evaluated. The dose and therapeutic effect of VPAs-miR and NPs-miR shall be determined in an acute murine model of IM. The possible functional improvement will be analysed by echocardiography and its proper remodeling by histological analysis. This project has been designed to evaluate a novel therapy for the treatment of IM, based on the over-expression of therapeutic miRNAs through the application of gene therapy and nanotechnology. (English) / rank | |||||||||||||||
Normal rank | |||||||||||||||
| Property / summary: The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic possibilities for the treatment of IM, based on the application of gene therapy and nanotechnology. First, the therapeutic role of microRNAs in the suppression of fibrosis (miR-29b and miR-133a) and in the protection (miR-133a and miR-199a) and proliferation (miR-199a) of cardiomyocytes will be studied. For this purpose, these microRNAs will be overexpressed in vivo, using cardiotropic adenoassociated viral vectors (AAVs), built with specific promoters of cardiomyocytes or fibroblasts and adjustable by tetracycline. In addition, an alternative method for sustained microRNA expression based on the use of biocompatible and biodegradable PLGA-PEG nanoparticles (NPs) and functionalised with the RGD peptide will be evaluated. The dose and therapeutic effect of VPAs-miR and NPs-miR shall be determined in an acute murine model of IM. The possible functional improvement will be analysed by echocardiography and its proper remodeling by histological analysis. This project has been designed to evaluate a novel therapy for the treatment of IM, based on the over-expression of therapeutic miRNAs through the application of gene therapy and nanotechnology. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
| |||||||||||||||
Revision as of 17:20, 12 October 2021
Project Q3161197 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | EXPRESSION OF CARDIOMIRS BY ADENO-ASSOCIATED VECTORS AND FUNCTIONALISED NANOPARTICLES FOR THE TREATMENT OF MYOCARDIAL INFARCTION |
Project Q3161197 in Spain |
Statements
33,000.0 Euro
0 references
66,000.0 Euro
0 references
50.0 percent
0 references
1 January 2014
0 references
31 March 2017
0 references
FUNDACION PARA LA INVESTIGACION MEDICA APLICADA
0 references
42°49'6.42"N, 1°38'39.34"W
0 references
31201
0 references
La principal limitación para la regeneración del corazón tras el infarto de miocardio (IM) es la incapacidad del tejido cardiaco de autoregenerarase, derivando en una pérdida de células funcionales y finalmente en la completa pérdida de la función cardiaca. Estudios recientes han demostrado el papel clave que los microRNAs ejercen en la regulación de la expresión génica asi como su expresión aberrante en condiciones patológicas. El objetivo de este proyecto es explorar nuevas posibilidades terapéuticas para el tratamiento del IM, basadas en la aplicación de la terapia génica y la nanotecnología. En primer lugar, se estudiará el papel terapéutico de los microRNAs en la supresión de fibrosis (miR-29b y miR-133a) y en la protección (miR-133a y miR-199a) y proliferación (miR-199a) de cardiomiocitos. Para ello, estos microRNAs se sobreexpresarán in vivo, mediante el uso de vectores virales adenoasociados (AAVs) cardiotrópicos, construídos con promotores específicos de cardiomiocitos o fibroblastos y regulables por tetraciclina. Además, se evaluará un método alternativo para la expresión sostenida de microRNAs basado en el uso de nanopartículas (NPs) de PLGA-PEG biocompatibles y biodegradables y funcionalizadas con el péptido RGD. La dosis y el efecto terapéutico de los AAVs-miR y las NPs-miR se determinarán en un modelo murino de IM agudo. La posible mejora funcional se analizará por ecocardiografía y su adecuado remodelado mediante análisis histológico. Este proyecto se ha diseñado para evaluar una terapia novedosa para el tratamiento del IM, basada en la sobre-expresión de miRNAs terapéuticos mediante la aplicación de la terapia génica y la nanotecnología. (Spanish)
0 references
The main limitation for the regeneration of the heart after myocardial infarction (MI) is the inability of the cardiac tissue to autoregenerase, resulting in a loss of functional cells and finally in the complete loss of cardiac function. Recent studies have shown the key role microRNAs play in regulating gene expression as well as their aberrant expression under pathological conditions. The aim of this project is to explore new therapeutic possibilities for the treatment of IM, based on the application of gene therapy and nanotechnology. First, the therapeutic role of microRNAs in the suppression of fibrosis (miR-29b and miR-133a) and in the protection (miR-133a and miR-199a) and proliferation (miR-199a) of cardiomyocytes will be studied. For this purpose, these microRNAs will be overexpressed in vivo, using cardiotropic adenoassociated viral vectors (AAVs), built with specific promoters of cardiomyocytes or fibroblasts and adjustable by tetracycline. In addition, an alternative method for sustained microRNA expression based on the use of biocompatible and biodegradable PLGA-PEG nanoparticles (NPs) and functionalised with the RGD peptide will be evaluated. The dose and therapeutic effect of VPAs-miR and NPs-miR shall be determined in an acute murine model of IM. The possible functional improvement will be analysed by echocardiography and its proper remodeling by histological analysis. This project has been designed to evaluate a novel therapy for the treatment of IM, based on the over-expression of therapeutic miRNAs through the application of gene therapy and nanotechnology. (English)
12 October 2021
0 references
Pamplona/Iruña
0 references
Identifiers
PI13_02144
0 references