Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra
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Fecha
2018
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Profesor/a Guía
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Idioma
es
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Universidad Andrés Bello
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Licencia CC
Licencia CC
Resumen
En mamíferos, la migración de neutrófilos durante un proceso de inflamación está
regulada por la vía de señalización GCSF-GCSFR. Esta citoquina y su receptor permiten la
salida de los neutrófilos desde los tejidos hematopoyéticos después de un daño estéril. En
pez cebra, Gcsf-Chr19 controla el proceso mencionado anteriormente, pero se desconoce
si esta citoquina se une a Gcsfr para ello. Además, el receptor Cxcr2 también participa en
este proceso regulando la entrada de neutrófilos a los vasos sanguíneos, pero en
presencia de patógenos. Debido a las posibles diferencias en las vías de señalización que
regulan la inflamación por daños estériles y aquellas provocadas por patógenos, además
de la posible diferencia entre mamíferos y peces, determinamos la función de Cxcr2 y
Gscfr en la migración de neutrófilos a través de los vasos sanguíneos después de un daño
estéril.
Para ello realizamos dos tipos de daños estériles (severo y leve) en larvas de pez cebra
Tg(Bacmpx:GFP)i114. Donde desarrollamos análisis de falta función ya sea por la
microinyección de un morfolino contra Gcsfr o por la incubación con SB225002 (inhibidor
químico de Cxcr2) y monitoreamos la migración de neutrófilos a distintas regiones de
interés durante 3 horas.
Nuestros resultados indicaron que Cxcr2 favorece la entrada de los neutrófilos a los
vasos sanguíneos, así como también la llegada de estos al área inflamada en el caso de
un daño estéril. Con respecto a Gcsfr nuestros resultados indican que este receptor no
participa en la entrada de los neutrófilos a los vasos sanguíneos al desencadenarse un
daño estéril, pero si está involucrado indirectamente en la direccionalidad de éstos al área
dañada.
In mammals, the migration of neutrophils during an inflammation process is regulated by the GCSF-GCSFR signaling pathway. This cytokine and its receptor allow the exit of neutrophils from hematopoietic tissues after sterile damage. In zebrafish, Gcsf-Chr19 controls the process mentioned above, but it is unknown if this cytokine binds to Gcsfr for it. In addition, the Cxcr2 receptor also participates in this process by regulating the entry of neutrophils into the blood vessels, but in the presence of pathogens. Due to the possible differences in the signaling pathways that regulate inflammation due to sterile damage and those caused by pathogens, in addition to the possible difference between mammals and fish, we determine the function of Cxcr2 and Gscfr in the migration of neutrophils through the blood vessels after sterile damage. To achieve this goal, we performed two types of sterile damage (severe and mild) in larvae of zebrafish Tg (Bacmpx: GFP) i114. Where we developed lack function analysis either by the microinjection of a morpholino against Gcsfr or by incubation with SB225002 (chemical inhibitor of Cxcr2) and we monitored the migration of neutrophils to different regions of interest for 3 hours. Our results indicated that Cxcr2 favors the entry of neutrophils into the blood vessels, as well as the arrival of these to the inflamed area in the case of sterile damage. With respect to Gcsfr our results indicate that this receptor does not participate in the entry of neutrophils into the blood vessels when sterile damage is unleashed, but is indirectly involved in the directionality of these to the damaged area.
In mammals, the migration of neutrophils during an inflammation process is regulated by the GCSF-GCSFR signaling pathway. This cytokine and its receptor allow the exit of neutrophils from hematopoietic tissues after sterile damage. In zebrafish, Gcsf-Chr19 controls the process mentioned above, but it is unknown if this cytokine binds to Gcsfr for it. In addition, the Cxcr2 receptor also participates in this process by regulating the entry of neutrophils into the blood vessels, but in the presence of pathogens. Due to the possible differences in the signaling pathways that regulate inflammation due to sterile damage and those caused by pathogens, in addition to the possible difference between mammals and fish, we determine the function of Cxcr2 and Gscfr in the migration of neutrophils through the blood vessels after sterile damage. To achieve this goal, we performed two types of sterile damage (severe and mild) in larvae of zebrafish Tg (Bacmpx: GFP) i114. Where we developed lack function analysis either by the microinjection of a morpholino against Gcsfr or by incubation with SB225002 (chemical inhibitor of Cxcr2) and we monitored the migration of neutrophils to different regions of interest for 3 hours. Our results indicated that Cxcr2 favors the entry of neutrophils into the blood vessels, as well as the arrival of these to the inflamed area in the case of sterile damage. With respect to Gcsfr our results indicate that this receptor does not participate in the entry of neutrophils into the blood vessels when sterile damage is unleashed, but is indirectly involved in the directionality of these to the damaged area.
Notas
Tesis (Magíster en Biotecnología)
Palabras clave
Neutrófilos, Receptor CXCR2, Receptor GCSFR