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El Factor Regulador de Interferón 4 inhibe la formación de neointima mediante la activación de la señalización del

Wen-Lin Cheng¹, Zhi-Gang She¹, Juan-Juan Qin¹

¹From Department of Cardiology, Renmin Hospital of Wuhan University, China (W.-L.C., Z.-G.S., F.-H.G., S.T., X.-Y.Z., Z.-H.W., H.L.); Basic Medical School (W.-L.C., Z.-G.S., J.-J.Q., J.-H.G., F.-H.G., P.Z., C.F., S.T., X.-Y.Z., J.G., Z.-H.W., Z.H., H.L.), Medical Research Institute, School of Medicine (W.-L.C., Z.-G.S., J.-J.Q., J.-H.G., F.-H.G., P.Z., C.F., S.T., X.-Y.Z., J.G., Z.-H.W., Z.H., H.L.), and College of Life Science (J.G., Z.H.), Wuhan University, China; and Institute of Model Animal of Wuhan University, China (W.-L.C., Z.-G.S., J.-J.Q., J.-H.G., F.-H.G., P.Z., C.F., S.T., X.-Y.Z., J.G., Z.-H.W., Z.H., H.L.).

|August 31, 2017

Resumen

El factor regulador del interferón 4 (IRF4) protege contra la restenosis arterial mediante la promoción de la expresión del factor de tipo Krüppel 4 (KLF4). Esta vía IRF4-KLF4 es crucial para prevenir la formación de neointima y puede ofrecer un objetivo terapéutico.

Área de la Ciencia:

Biología cardiovascular
Inmunología
La medicina molecular

Sus antecedentes:

Los mecanismos de formación de neointima no se comprenden completamente.
Los factores reguladores del interferón (FRI) son reguladores inmunológicos clave en las enfermedades cardiometabólicas.
Actualmente se desconoce el papel de IRF4 en la restenosis arterial.

Objetivo del estudio:

Investigar el papel y el mecanismo de IRF4 en la formación de neointima.
Para explorar la relación entre IRF4 y el factor similar a Krüppel 4 (KLF4) en la restenosis arterial.
Determinar si el eje IRF4-KLF4 es un objetivo terapéutico potencial para la reestenosis arterial.

Principales métodos:

Análisis de la expresión de IRF4 en las arterias restenóticas de humanos y ratones.
Evaluación de la formación de neointima en modelos de ratón y ratón transgénicos con knockout de IRF4 y con células de músculo liso (SMC) específicas.
Identificación de objetivos intermedios de IRF4 mediante microarrays, bioinformática y ensayos de inmunoprecipitación de la cromatina.
Evaluación de la dependencia de KLF4 del efecto de IRF4 en la formación de neointima y el cambio de fenotipo de SMC.

Principales resultados:

La expresión de IRF4 está regulada a la baja en las arterias restenóticas.
La deficiencia de IRF4 potencia la formación de neointima, mientras que la sobreexpresión de IRF4 la inhibe, principalmente en las SMC.
IRF4 promueve directamente la expresión de KLF4, y esta interacción es esencial para los efectos protectores de IRF4.
IRF4 promueve la desdiferenciación y migración de SMC, pero su efecto general es protector contra la formación de neointima a través de KLF4.

Conclusiones:

IRF4 protege contra la formación de neointima arterial mediante la regulación de la expresión de KLF4 a través de la unión directa con el promotor.
El eje IRF4-KLF4 identificado es un regulador crítico de la patología vasculoproliferativa.
Dirigirse a la vía IRF4-KLF4 presenta una estrategia terapéutica prometedora para la restenosis arterial.

Palabras clave:

Factores de transcripción similares a los de Kruppel Proliferación de las células Restenosis de las arterias coronarias Factor de regulación del interferón-4 células del músculo liso

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