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Deficiencia hematopoyética del ARN largo no codificante MALAT1 Promueve la aterosclerosis y la inflamación de la

Sebastian Cremer^1,2, Katharina M Michalik¹, Ariane Fischer¹

¹Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Frankfurt, Germany (S.C., K.M.M., A.F., L.P., N.J., R.A.B., M.M.-R., D.J., S.U., S.D.).

|December 28, 2018

Resumen

Los niveles reducidos del ARN largo no codificante MALAT1 empeoran la aterosclerosis al aumentar la acumulación de células inflamatorias en ratones y humanos. Un MALAT1 más bajo indica un peor pronóstico para la enfermedad aterosclerótica.

Área de la Ciencia:

Biología molecular
Investigación cardiovascular
La genómica

Sus antecedentes:

Los ARN largos no codificantes (ARNlnc) juegan un papel en la regulación génica, incluido el control epigenético.
La transcripción 1 del adenocarcinoma pulmonar asociado a la metástasis (MALAT1) es un lncRNA con diversas funciones.
El papel de MALAT1 en la aterosclerosis, una enfermedad cardiovascular, era en gran parte inexplorado.

Objetivo del estudio:

Investigar el impacto del lncRNA MALAT1 en el desarrollo de la aterosclerosis.
Para determinar si MALAT1 influye en el comportamiento inflamatorio de las células en el contexto de la aterosclerosis.

Principales métodos:

Se estudió la aterosclerosis en ratones con deficiencia de apolipoproteína E (Apoe-/-) y con deficiencia de MALAT1- (Malat1-/-) en una dieta alta en grasas.
Se realizaron experimentos de trasplante de médula ósea para evaluar el papel de las células hematopoyéticas.
La expresión de MALAT1 fue analizada en placas ateroscleróticas humanas.

Principales resultados:

Los ratones que carecían de MALAT1 presentaban placas ateroscleróticas más grandes y una mayor infiltración de células inflamatorias.
Las células hematopoyéticas de ratones con deficiencia de MALAT1 mostraron una mayor adhesión y liberación de mediadores proinflamatorios.
La reducción de los niveles de MALAT1 en las placas humanas se correlacionó con la gravedad de la enfermedad y un peor pronóstico.

Conclusiones:

La disminución de los niveles de MALAT1 exacerba la formación y progresión de la lesión aterosclerótica.
Los efectos pro-ateroscleróticos de la deficiencia de MALAT1 están mediados principalmente por la acumulación de células hematopoyéticas.
MALAT1 puede servir como un biomarcador potencial para la gravedad de la enfermedad aterosclerótica.

Palabras clave:

El ARN la aterosclerosis inflamación Leucócitos

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