Neuronal Phenotype of <i>col4a1</i> and <i>col25a1</i>: An Intriguing Hypothesis in Vertebrates Brain Aging

Collagens are the most abundant proteins in vertebrates and constitute the major components of the extracellular matrix. Collagens play an important and multifaceted role in the development and functioning of the nervous system and undergo structural remodeling and quantitative modifications during...

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Bibliographic Details
Main Authors: Adele Leggieri, Chiara Attanasio, Antonio Palladino, Paolo de Girolamo, Carla Lucini, Livia D’Angelo
Format: Article
Language:English
Published: MDPI AG 2022-02-01
Series:International Journal of Molecular Sciences
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Online Access:https://www.mdpi.com/1422-0067/23/3/1778
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Summary:Collagens are the most abundant proteins in vertebrates and constitute the major components of the extracellular matrix. Collagens play an important and multifaceted role in the development and functioning of the nervous system and undergo structural remodeling and quantitative modifications during aging. Here, we investigated the age-dependent regulation of <i>col4a1</i> and <i>col25a1</i> in the brain of the short-lived vertebrate <i>Nothobranchius furzeri</i>, a powerful model organism for aging research due to its natural fast-aging process and further characterized typical hallmarks of brain aging in this species. We showed that <i>col4a1</i> and <i>col25a1</i> are relatively well conserved during vertebrate evolution, and their expression significantly increases in the brain of <i>N. furzeri</i> upon aging. Noteworthy, we report that both <i>col4a1</i> and <i>col25a1</i> are expressed in cells with a neuronal phenotype, unlike what has already been documented in mammalian brain, in which only <i>col25a1</i> is considered a neuronal marker, whereas <i>col4a1</i> seems to be expressed only in endothelial cells. Overall, our findings encourage further investigation on the role of <i>col4a1</i> and <i>col25a1</i> in the biology of the vertebrate brain as well as the onset of aging and neurodegenerative diseases.
ISSN:1661-6596
1422-0067