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c-Jun disminuye la actividad del canal K (((+) dependiente de la tensión en las células del músculo liso de la
1Department of Medicine, University of California, San Diego, San Diego, CA 92103-8382, USA.
Circulation
|September 26, 2001
Resumen
El factor de transcripción c-Jun reduce la actividad de los canales de potasio dependientes de la tensión (K(v)) en las células del músculo liso de la arteria pulmonar (PASMC). Esta disminución en las corrientes K ((v) conduce a la despolarización de la membrana, al aumento del calcio y a una mayor proliferación de PASMC.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Fisiología cardiovascular fisiología cardiovascular.
- Biología celular Biología celular.
Sus antecedentes:
- Los canales de potasio (K ((v)) regulados por voltaje regulan el potencial de la membrana (E ((m))), lo que influye en la concentración de Ca ((2+) libre citosólico ([Ca ((2+) ]).
- El aumento de [Ca2+] en las células del músculo liso de la arteria pulmonar (PASMC) promueve la vasoconstricción y la proliferación.
- El papel de c-Jun, un factor de transcripción que estimula la proliferación, en la regulación de la actividad del canal K (v) en las PASMCs no estaba claro anteriormente.
Objetivo del estudio:
- Para investigar el efecto de c-Jun en la actividad del canal K (v) en PASMCs.
- Para determinar el impacto de c-Jun en el potencial de membrana y la proliferación de PASMC.
Principales métodos:
- Se utilizaron vectores adenovirales para sobreexpresar c-Jun en PASMCs de cultivo primario.
- Las corrientes K (I) y K (V) se midieron utilizando electrofisiología.
- La RT-PCR de una sola célula evaluó los niveles de Kv1.5 mRNA, y la incorporación de [3H]timidina midió la proliferación.
Principales resultados:
- La sobreexpresión de c-Jun disminuyó las corrientes K(v) y los niveles de Kv1.5 de ARNm en PASMCs.
- c-Jun upregulated Kvbeta(2) expresión de la proteína y acelerado I(K(V)) inactivación.
- Los PASMCs que sobreexpresan c-Jun exhiben despolarización de la membrana y aumento de la proliferación.
Conclusiones:
- La proliferación de PASMC mediada por c-Jun está relacionada con la reducción de la actividad del canal K.
- La disminución de las corrientes K (v) resulta en la despolarización de la membrana, elevando el [Ca2+] (cyt).
- Este mecanismo mejora el crecimiento de PASMC, lo que sugiere un papel para c-Jun en la hipertensión pulmonar.
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