Linked Life Data

19170165

Source:http://linkedlifedata.com/resource/pubmed/id/19170165

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2009-4-20
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1097-4547
pubmed:author
pubmed:copyrightInfo
(c) 2009 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1858-70
pubmed:meshHeading
pubmed-meshheading:19170165-Animals, pubmed-meshheading:19170165-Cell Membrane, pubmed-meshheading:19170165-Ganglia, Spinal, pubmed-meshheading:19170165-Gastric Inhibitory Polypeptide, pubmed-meshheading:19170165-Gene Expression Regulation, pubmed-meshheading:19170165-Growth Cones, pubmed-meshheading:19170165-Immunohistochemistry, pubmed-meshheading:19170165-Male, pubmed-meshheading:19170165-Mice, pubmed-meshheading:19170165-Mice, Inbred C57BL, pubmed-meshheading:19170165-Mice, Knockout, pubmed-meshheading:19170165-Nerve Regeneration, pubmed-meshheading:19170165-RNA, Messenger, pubmed-meshheading:19170165-Rats, pubmed-meshheading:19170165-Rats, Wistar, pubmed-meshheading:19170165-Receptors, Gastrointestinal Hormone, pubmed-meshheading:19170165-Schwann Cells, pubmed-meshheading:19170165-Sciatic Nerve, pubmed-meshheading:19170165-Sciatic Neuropathy, pubmed-meshheading:19170165-Sensory Receptor Cells, pubmed-meshheading:19170165-Spinal Cord
pubmed:year
2009
pubmed:articleTitle
Glucose-dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): cellular localization, lesion-affected expression, and impaired regenerative axonal growth.
pubmed:affiliation
Molecular Neurobiology Laboratory, Department of Neurology, Heinrich-Heine-University of Düsseldorf, Düsseldorf, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't