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La edición de genes ofrece una curación para algunos trastornos de la sangre
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La edición de genes ofrece una curación para algunos trastornos de la sangre

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La edición de genes ofrece una curación para algunos trastornos de la sangre

Investigadores de la  Universidad Nueva  de Gales del Sure en Australia han demostrado que el cambio de una sola letra del ADN de los glóbulos rojos de la sangre humana aumenta su producción de la hemoglobina que transporta el oxígeno, un avance que podría conducir a una cura para la anemia de células falciformes y otros trastornos de la sangre.

La nueva técnica de edición del genoma, en el que se introduce una mutación genética de origen natural beneficiosa en las células, funciona mediante la activación de un gen durmiente, que sí está activo en el útero pero se encuentra apagado en la mayoría de personas después del nacimiento. "Estamos en una era fascinante con la edición del genoma", señala Merlin Crossley, y ahora ya podemos cortar y reparar con precisión genes. Y, añade, nuestro estudio proporciona una prueba de concepto de que cambiar una sola letra del ADN en un gen podría aliviar los síntomas de la anemia de células falciformes y talasemia. Y, además, debido que la variación genética introducida ya existe, este enfoque debe ser eficaz y seguro, aunque reconoce que se necesita más investigación antes de que pueda ser probado en personas como una posible cura para enfermedades graves de la sangre.

El estudio se publica en la revista Nature Communications

Las personas producimos dos tipos diferentes de hemoglobina. «Durante la fase de desarrollo en el útero, el gen de la hemoglobina fetal está activado.

Esto produce la hemoglobina fetal, que tiene una alta afinidad por el oxígeno, lo que permite al bebé a extraer el oxígeno de la sangre de su madre», explica Crossley. Sin embargo, después de nacer, el gen de la hemoglobina fetal se apaga y se enciende el de la hemoglobina adulta.

Las mutaciones que afectan a la hemoglobina adulta se encuentran entre los más comunes de todas las mutaciones genéticas humanas, ya que se calcula que alrededor del 5 % de la población mundial es portadora de un gen de la hemoglobina adulta defectuoso. Las personas que heredan dos genes mutantes -uno de su madre y uno de su padre- sufren enfermedades mortales como la anemia de células falciformes y la talasemia, que requieren tratamiento de por vida con transfusiones de sangre y medicamentos.

Gen de la hemoglobina

Los investigadores han basado su nuevo enfoque en el hecho de que un pequeño número de personas con daño en la hemoglobina adulta tiene una mutación adicional, beneficiosa, en el gen de la hemoglobina fetal. Esta mutación beneficiosa mantiene su gen de la hemoglobina fetal encendido para el resto de su vida y reduce los síntomas de manera significativa, dice Crossley.

Los investigadores introdujeron esta mutación de una sola letra en los glóbulos rojos humanos mediante la edición de genes. Las roturas en el ADN pueden ser letales para las células, por lo que tienen la maquinaria construida para reparar cualquier daño lo más pronto posible, señala Crossley.

Y nosotros hemos aprovechado este efecto. Cuando nuestra proteína de edición genoma corta el ADN, la célula rápidamente lo reemplaza con el ADN de los donantes que también hemos proporcionado.

La técnica, si finalmente muestra que es eficaz y segura, ofrecería ventajas significativas sobre otros enfoques, como la terapia génica convencional, en la que los virus se utilizan para transportar genes sanos celda para reemplazar el gen defectuoso. Mayo 25 / 2015 (abc-salud),

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