Regulación de la mecanotransducción de los cardiomiocitos por el ciclo cardíaco
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K Yamamoto1, Q N Dang, Y Maeda
1Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Circulation
|March 14, 2001
Resumen
El estrés mecánico durante el ciclo cardíaco activa vías de señalización específicas. Esta mecanotransducción celular puede explicar cómo la presión y la sobrecarga de volumen afectan de manera diferente a la morfología cardíaca.
Área de la Ciencia:
- Cardiología Cardiología.
- Biología Molecular Biología Molecular
- La biofísica es la biofísica.
Sus antecedentes:
- La sobrecarga de presión del ventrículo izquierdo (sistólica) y la sobrecarga de volumen (diastólica) inducen respuestas morfológicas distintas.
- Comprender los mecanismos celulares que subyacen a estas respuestas es crucial para la salud cardíaca.
Objetivo del estudio:
- Investigar cómo la tensión mecánica durante las diferentes fases del ciclo cardíaco afecta la señalización de los cardiomiocitos y la expresión génica.
- Para determinar si el tiempo del ciclo cardíaco influye en la respuesta celular al estrés mecánico.
Principales métodos:
- Un nuevo sistema controlado por computadora aplicó una tensión biaxial a los cardiomiocitos durante fases específicas del ciclo cardíaco (sistólico vs. diastólico).
- Medición de la activación de las vías de la proteína quinasa activada por mitógeno (MAPK) (p44/42, p38, JNK) y de la síntesis de genes y proteínas.
Principales resultados:
- La cepa sistólica activó selectivamente p44/42 MAPK y MAPK / proteína quinasa quinasa regulada por la señal extracelular (MEK1/2) en comparación con la cepa diastólica.
- Tanto el péptido natriurético cerebral como la expresión de ARNm de tenascina-C fueron significativamente más altos con la tensión sistólica.
- La síntesis de proteínas, medida por la incorporación de [(3) H]leucina, fue mayor con la tensión sistólica e inhibida por un inhibidor MEK1/2.
Conclusiones:
- La activación mecánica de p44/42 MAPK/MEK1/2, la expresión génica y la síntesis de proteínas está regulada por el ciclo cardíaco.
- La mecanotransducción cardíaca durante fases específicas del ciclo puede ser la base de los efectos diferenciales de la presión y la sobrecarga de volumen en el corazón.
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