Aging preferentially affects molecular pathways implicated in development and disease of myelinating glial cells

Détails

ID Serval
serval:BIB_FB0C6D90E840
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Institution
Titre
Aging preferentially affects molecular pathways implicated in development and disease of myelinating glial cells
Titre de la conférence
Meeting of the Peripheral Nerve Society
Auteur(s)
Verdier V., Csardi G., de Preux-Charles A.-.S., Medard J.-.J., Bergmann S., Verheijen M., Charst R.
Adresse
Potomac, Maryland, June 25-29, 2011
ISBN
1085-9489
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
16
Série
Journal of the Peripheral Nervous System
Pages
S143-S143
Langue
anglais
Notes
Publication type : Meeting Abstract
Résumé
The central and peripheral nervous systems are involved in multiple age-dependent neurological deficits that are often attributed to alterations in function of myelinating glial cells. However, the molecular events that underlie the age-related decline of glial cell function are unknown. We used Schwann cells as a model to study biological processes affected in glial cells by aging. We comprehensively profiled gene expression of the Schwann cellrich mouse sciatic nerve throughout life, from day of birth until senescence (840 days of age). We combined the aging data with the microarray transcriptional data obtained using nerves isolated from Schwann cell-specific neuropathy-inducing mutants MPZCre/+/Lpin1fE2−3/fE2−3 , MPZCre/+/ScapfE1/fE1 and Pmp22-null mice. The majority of age related transcripts were also affected in the analyzed mouse models of neuropathy (54.4%) and in development (59.5%) indicating a high level of overlapping in implicated molecular pathways. We observed that compared to peripheral nerve development, dynamically changing expression profiles in aging have opposite (anticorrelated) orientation while they copy the orientation of transcriptional changes observed in analyzed neuropathy models. Subsequent clustering and biological annotation of dynamically changing transcripts revealed that the processes most significantly deregulated in aging include inflammatory/immune response and lipid biosynthesis/metabolism. Importantly, the changes in these pathways were also observed in myelinated oligodendrocyte-rich optic nerves of aged mice, albeit with lower magnitude. This observation suggests that similar biological processes are affected in aging glial cells in central and peripheral nervous systems, however with different dynamics. Our data, which provide the first comprehensive comparison of molecular changes in glial cells in three distinct biological conditions comprising development, aging and disease, provide not only a new inside into the molecular alterations underlying neural system aging but also identify target pathways for potential therapeutic approaches to prevent or delay complications associated with age-related and inherited forms of neuropathies. *Current address: Department of Physiology, UCSF, San Francisco, CA, USA.
Web of science
Création de la notice
01/09/2011 9:50
Dernière modification de la notice
20/08/2019 17:26
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