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La prostaglandina microsomal e2 sintasa-1 modula la respuesta a las lesiones vasculares
Miao Wang1, Kaori Ihida-Stansbury, Devashish Kothapalli
1Institute for Translational Medicine and Therapeutics, Department of Pharmacology, University of Pennsylvania, Philadelphia, USA. miaowang@upenn.edu
Circulation
|February 2, 2011
Resumen
Dirigirse a la prostaglandina E sintasa-1 microsomal (mPGES-1) reduce la lesión vascular y la hiperplasia mediante la regulación de la tenascina-C. Esto sugiere que los inhibidores de mPGES-1 pueden ayudar a la terapia de intervención coronaria percutánea.
Área de la Ciencia:
- Ciencias biomédicas Ciencias biomédicas.
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
- Inflamación e inmunología.
Sus antecedentes:
- La prostaglandina E sintasa-1 microsomal (mPGES-1) produce la prostaglandina E2 (PGE2).Esto es lo que hace que las prostaglandinas E2 sean más potentes.
- La inhibición de mPGES-1 puede ofrecer alternativas más seguras a los inhibidores de la COX-2, evitando la hipertensión y la trombosis.
- La deleción de mPGES-1 ha demostrado efectos protectores contra la aterosclerosis y la formación de aneurismas aórticos.
Objetivo del estudio:
- Para investigar el papel de mPGES-1 en la respuesta a la lesión vascular.
- Para determinar el efecto de la deleción de mPGES-1 en la hiperplasia neointimal.
- Explorar los mecanismos subyacentes que involucran la tenascina-C y la producción de prostaglandinas.
Principales métodos:
- Modelo de lesión por alambre de la arteria femoral en ratones tipo salvaje y nocaut de mPGES-1.
- Cuantificación del área neoinimal y la estenosis vascular.
- Análisis de la expresión de tenascina-C y la biosíntesis de las prostaglandinas (PGE2, PGI2) en el tejido y las células vasculares.
Principales resultados:
- Los ratones knockout de mPGES-1 exhibieron un área neointimal significativamente reducida y estenosis vascular después de la lesión.
- La inducción de tenascina-C después de la lesión se atenuó en ratones knockout de mPGES-1.
- Las células del músculo liso vascular que carecen de mPGES-1 producen menos PGE2 y más PGI2, suprimiendo la proliferación y la migración.
Conclusiones:
- La deleción de mPGES-1 atenúa la hiperplasia neointimal después de una lesión vascular.
- El mecanismo implica la regulación de la expresión de la tenascina-C.
- Los inhibidores de mPGES-1 representan una terapia adyuvante potencial para la intervención coronaria percutánea.
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