Zebrafish, a diurnal vertebrate characterized by gradual senescence, is an excellent model for studying age-dependent diseases, such as neurodegenerative diseases. Cerebral amyloid angiopathy (CAA) caused by amyloid β (Aβ) deposition around brain microvessels is a human neurovascular degenerative disease that is characterized by an early onset of recurrent stroke episodes, vascular brain degenerative changes, and moderate to severe clinical presentations. Recently, by using the zebrafish model, we investigated whether Aβ peptides cause endothelial cells to enter senescence at an early stage of vascular development. During early embryonic zebrafish development, the presence of senescence-associated biomarkers, such as β-galactosidase and the cyclin-dependent kinase inhibitor p21, has been shown to be predictive of the premature aging phenotype. By measuring β-galactosidase activity and p21 expression in whole-mount zebrafish embryos exposed to Aβ, we demonstrated that these oxidative peptides promote vascular senescence at an early stage of development, a harbinger of vascular clinical symptoms in adult. This chapter describes the methods for studying cell senescence in zebrafish, detailing protocols for β-gal activity and the in situ p21 hybridization in whole-mount zebrafish embryos.

Donnini, S., Giachetti, A., Ziche, M. (2013). Assessing vascular senescence in zebrafish.. In Cell Senescence (pp. 517-531). Galluzzi L., Vitale I., Kepp O., Kroemer G. [10.1007/978-1-62703-239-1_34].

Assessing vascular senescence in zebrafish.

DONNINI, SANDRA;ZICHE, MARINA
2013

Abstract

Zebrafish, a diurnal vertebrate characterized by gradual senescence, is an excellent model for studying age-dependent diseases, such as neurodegenerative diseases. Cerebral amyloid angiopathy (CAA) caused by amyloid β (Aβ) deposition around brain microvessels is a human neurovascular degenerative disease that is characterized by an early onset of recurrent stroke episodes, vascular brain degenerative changes, and moderate to severe clinical presentations. Recently, by using the zebrafish model, we investigated whether Aβ peptides cause endothelial cells to enter senescence at an early stage of vascular development. During early embryonic zebrafish development, the presence of senescence-associated biomarkers, such as β-galactosidase and the cyclin-dependent kinase inhibitor p21, has been shown to be predictive of the premature aging phenotype. By measuring β-galactosidase activity and p21 expression in whole-mount zebrafish embryos exposed to Aβ, we demonstrated that these oxidative peptides promote vascular senescence at an early stage of development, a harbinger of vascular clinical symptoms in adult. This chapter describes the methods for studying cell senescence in zebrafish, detailing protocols for β-gal activity and the in situ p21 hybridization in whole-mount zebrafish embryos.
Donnini, S., Giachetti, A., Ziche, M. (2013). Assessing vascular senescence in zebrafish.. In Cell Senescence (pp. 517-531). Galluzzi L., Vitale I., Kepp O., Kroemer G. [10.1007/978-1-62703-239-1_34].
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/46616
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo