Comparative analysis of Krüppel-like factors expression in the retinas of zebrafish and mice during development and after injury


Por: Avila-Mendoza, J, Urban-Sosa, VA, Lazcano, I, Orozco, A, Luna, M, Martínez-Moreno, CG, Arámburo, C

Publicada: 15 sep 2024 Ahead of Print: 1 jul 2024
Resumen:
The Kr & uuml;ppel-like factors (KLFs) have emerged as important transcriptional regulators of various cellular processes, including neural development. Some of them have been described as intrinsic factors involved in axon regeneration in the central nervous system (CNS) of vertebrates. Zebrafish are known for their ability to regenerate several tissues in adulthood, including the CNS, a capability lost during vertebrate evolution and absent in adult mammals. The role that KLFs could play in this differential ability remains unknown. Therefore, in this study, we analyzed the endogenous response of certain KLFs implicated in axon regeneration (KLFs 6, 7, 9, and 13) during retina development and after axon injury. The results showed that the expression of Klfs 6 , 7 , and 13 decreases in the developing retina of mice but not in zebrafish, while the mRNA levels of Klf9 strongly increase in both species. The response to injury was further analyzed using optic nerve crush (ONC) as a model of lesion. Our analysis during the acute phase (hours) demonstrated an induction of Klfs 6 and 7 expression exclusively in the zebrafish retina, while Klfs 9 and 13 mRNA levels increased in both species. Further analysis of the chronic response (days) showed that mRNA levels of Klf6 transiently increase in the retinas of both zebrafish and mice, whereas those of Klf7 decrease later after optic nerve injury. In addition, the analysis revealed that the expression of Klf9 decreases, while that of Klf13 increases in the retinas of zebrafish in response to optic nerve injury but remains unaltered in mice . Altogether, these findings support the hypothesis that KLFs may play a role in the differential axon regeneration abilities exhibited by fish and mice.

Filiaciones:
Avila-Mendoza, J:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Urban-Sosa, VA:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Lazcano, I:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Orozco, A:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Luna, M:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Martínez-Moreno, CG:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico

Arámburo, C:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Mol & Celular, Campus Juriquilla, Queretaro 76230, Mexico
ISSN: 00166480
Editorial
Academic Press Inc., 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 356 Número:
Páginas:
WOS Id: 001266089700001
ID de PubMed: 38964422
imagen hybrid, All Open Access; Hybrid Gold Open Access