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Un vínculo inesperado entre un antibiótico, los canales de pannexina y la apoptosis
Ivan K H Poon1, Yu-Hsin Chiu2, Allison J Armstrong3
11] The Center for Cell Clearance, University of Virginia, Charlottesville, Virginia 22908, USA [2] Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia 22908, USA [3] Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA [4] La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria 3086, Australia.
Nature
|March 21, 2014
Resumen
El antibiótico trovafloxacina inhibe los canales pannexin 1 (PANX1), cruciales para el desmontaje celular durante la apoptosis. Este descubrimiento vincula los antibióticos con la integridad celular y puede guiar el desarrollo de nuevos fármacos antibacterianos.
Área de la Ciencia:
- Biología celular Biología celular.
- Farmacología Farmacología.
- Microbiología Microbiología.
Sus antecedentes:
- Los canales pannexin 1 de la membrana plasmática (PANX1) median la liberación de señales de "encuéntrame" de las células apoptóticas, atrayendo a los fagocitos para su depuración.
- La clase de antibióticos quinolona es ampliamente utilizada para las infecciones bacterianas, pero algunos tienen efectos secundarios graves e inexplicables.
- El aumento de las bacterias resistentes a los fármacos requiere el desarrollo de nuevas estrategias terapéuticas y una mejor comprensión de los mecanismos de los antibióticos.
Objetivo del estudio:
- Para identificar nuevos inhibidores de los canales de la pannexina 1 (PANX1).
- Para investigar el papel de PANX1 en el desmontaje celular durante la apoptosis.
- Explorar el vínculo potencial entre la estructura del antibiótico, la inhibición de PANX1 y la integridad celular.
Principales métodos:
- Se empleó una pantalla de moléculas pequeñas para identificar inhibidores de la PANX1.
- La interacción directa de Trovafloxacina con PANX1 se evaluó en concentraciones fisiológicamente relevantes.
- Se analizaron los efectos de la inhibición de PANX1 y el nocaut genético en la fragmentación celular apoptótica.
Principales resultados:
- La trovafloxacina fue identificada como un nuevo inhibidor de los canales de la pannexina 1 (PANX1).
- La inhibición de PANX1 por trovafloxacina interrumpió la fragmentación normal de las células apoptóticas.
- La deleción genética de PANX1 imitaba los defectos de desmontaje celular observados con el tratamiento con trovafloxacina.
Conclusiones:
- Los canales Pannexin 1 (PANX1) juegan un papel crítico y no redundante en la regulación del desmontaje celular durante la apoptosis.
- La trovafloxacina se dirige directamente a PANX1 en concentraciones terapéuticas, vinculando este antibiótico a la integridad celular.
- Las características estructurales de las quinolonas pueden influir en la inhibición de la PANX1, lo que sugiere el potencial para la reingeniería de antibióticos para mitigar los efectos secundarios y desarrollar nuevos agentes antibacterianos.
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