Glucose-dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): cellular localization, lesion-affected expression, and impaired regenerative axonal growth.

Détails

ID Serval
serval:BIB_4A9CD880C6FC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Glucose-dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): cellular localization, lesion-affected expression, and impaired regenerative axonal growth.
Périodique
Journal of Neuroscience Research
Auteur(s)
Buhren B.A., Gasis M., Thorens B., Müller H.W., Bosse F.
ISSN
1097-4547[electronic], 0360-4012[linking]
Statut éditorial
Publié
Date de publication
2009
Volume
87
Numéro
8
Pages
1858-1870
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Glucose-dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up-regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion-induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT-PCR. Our results clearly identified lesion-induced as well as tissue type-specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane-associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type-specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR-deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR-deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild-type mice.
Mots-clé
Animals, Cell Membrane/metabolism, Cell Membrane/ultrastructure, Ganglia, Spinal/metabolism, Ganglia, Spinal/physiopathology, Gastric Inhibitory Polypeptide/genetics, Gastric Inhibitory Polypeptide/metabolism, Gene Expression Regulation/genetics, Growth Cones/metabolism, Growth Cones/ultrastructure, Immunohistochemistry, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nerve Regeneration/physiology, RNA, Messenger/metabolism, Rats, Rats, Wistar, Receptors, Gastrointestinal Hormone/genetics, Receptors, Gastrointestinal Hormone/metabolism, Schwann Cells/cytology, Schwann Cells/metabolism, Sciatic Nerve/injuries, Sciatic Nerve/metabolism, Sciatic Neuropathy/metabolism, Sciatic Neuropathy/physiopathology, Sensory Receptor Cells/cytology, Sensory Receptor Cells/metabolism, Spinal Cord/metabolism, Spinal Cord/physiopathology
Pubmed
Web of science
Création de la notice
14/07/2009 9:44
Dernière modification de la notice
20/08/2019 13:58
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