Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-9-3
pubmed:abstractText
The aim of this work was to determine whether the stimulating effect of glucagon-like peptide (GLP)-2 on astrocyte proliferation could be reinforced by proliferating substances, including growth factors such as EGF, platelet-derived growth factor, insulin-like growth factor type I (IGF-I) or a hormone such as insulin. Both DNA synthesis and astrocyte density, as well as the expression of c-Fos, Ki-67, proliferating cell nuclear antigen and glial fibrillary acidic proteins, were found to be higher in the presence of GLP-2 than in its absence. In an attempt to get a better understanding of this process, intracellular cyclic adenosine monophosphate (cAMP) production, extracellular signal-regulated kinase (ERK) 1/2 phosphorylation and the expression of GLP-2R and IGF-I receptor (IGF-IR) mRNAs were studied in response to growth factors. Our results indicate that, in the presence of different growth factors, GLP-2 does not increase cAMP production but raises ERK 1/2 phosphorylation. In addition, GLP-2R mRNA expression was increased by IGF-I, whilst mRNA expression of IGF-IR was higher in cells incubated with GLP-2 than in control cells. These results suggest for the first time that GLP-2 and several growth factors show synergistic effects on the proliferation of rat astrocytes, a process in which an enhanced expression of GLP-2R and IGF-IR may be involved, providing additional insights into the physiological role of this novel neuropeptide, specially during astroglial regeneration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/GLP-2 receptor, http://linkedlifedata.com/resource/pubmed/chemical/Glucagon-Like Peptide 2, http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I, http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides..., http://linkedlifedata.com/resource/pubmed/chemical/Platelet-Derived Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, IGF Type 1, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucagon
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0893-7648
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
183-93
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19672727-Animals, pubmed-meshheading:19672727-Astrocytes, pubmed-meshheading:19672727-Cell Division, pubmed-meshheading:19672727-Cells, Cultured, pubmed-meshheading:19672727-Drug Synergism, pubmed-meshheading:19672727-Epidermal Growth Factor, pubmed-meshheading:19672727-Gene Expression Regulation, pubmed-meshheading:19672727-Glucagon-Like Peptide 2, pubmed-meshheading:19672727-Hypoglycemic Agents, pubmed-meshheading:19672727-Insulin, pubmed-meshheading:19672727-Insulin-Like Growth Factor I, pubmed-meshheading:19672727-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:19672727-Platelet-Derived Growth Factor, pubmed-meshheading:19672727-RNA, Messenger, pubmed-meshheading:19672727-Rats, pubmed-meshheading:19672727-Receptor, IGF Type 1, pubmed-meshheading:19672727-Receptors, Glucagon, pubmed-meshheading:19672727-Up-Regulation
pubmed:year
2009
pubmed:articleTitle
Synergistic effect of glucagon-like peptide 2 (GLP-2) and of key growth factors on the proliferation of cultured rat astrocytes. Evidence for reciprocal upregulation of the mRNAs for GLP-2 and IGF-I receptors.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't