Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-12-29
pubmed:abstractText
Interleukin-6 (IL-6) is involved in a variety of biological responses, including the glucose metabolism and cell growth, which is a critical physiological function requiring multiple metabolic pathways. Therefore, in the present study, we examined the effect of IL-6 on 2-deoxyglucose (2-DG) uptake and the related signaling pathways in primary cultured chicken hepatocytes. IL-6 increased 2-DG uptake in a time- (> or =4 h) and a dose -(> or =5 ng/ml) dependent manner. Indeed, IL-6 increased GLUT-2 mRNA and protein expression as well as 2-DG uptake, which were blocked by actinomycin D (AD, transcription inhibitor) and cycloheximide (CHX, translation inhibitor). IL-6 (10 ng/ml) increased the level of IL-6Ralpha and glycoprotein (gp) 130 (IL-6Rbeta) protein expressions. IL-6 increased Janus Kinase (JAK)-2, signal transducer and activator of transcription (STAT)-3 phosphorylation, intracellular Ca(2+) concentration, and PKC phosphorylation. IL-6-induced increase of 2-DG uptake and GLUT-2 protein expression were blocked by JAK2-specific siRNA, a STAT3 inhibitor, staurosporine, and bisindolylmaleimide I (PKC inhibitors). In addition, IL-6 increased EGFR/src/FAK, PI3K/Akt phosphorylation and 2-DG uptake as well as GLUT-2 protein expression, which were blocked by AG 1478 (EGF receptor inhibitor), PP2 (src family of tyrosine kinase inhibitor), PI3K-specific siRNA, and a Akt inhibitor. Furthermore, IL-6 increased p44/42 MAPKs phosphorylation and p44 and p42 MAPK-specific siRNA mixture blocked IL-6-induced increase of 2-DG uptake and GLUT-2 protein expression. In conclusion, IL-6 stimulates the 2-DG uptake through p44/42 MAPKs activation via Ca(2+)/PKC and EGF receptor in primary cultured chicken hepatocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Deoxyglucose, http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP..., http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/STAT Transcription Factors
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1097-4652
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
218
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
643-52
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19006119-Animals, pubmed-meshheading:19006119-Calcium, pubmed-meshheading:19006119-Cells, Cultured, pubmed-meshheading:19006119-Chickens, pubmed-meshheading:19006119-Deoxyglucose, pubmed-meshheading:19006119-Enzyme Activation, pubmed-meshheading:19006119-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:19006119-Hepatocytes, pubmed-meshheading:19006119-Interleukin-6, pubmed-meshheading:19006119-Janus Kinases, pubmed-meshheading:19006119-Male, pubmed-meshheading:19006119-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:19006119-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:19006119-Models, Biological, pubmed-meshheading:19006119-Protein Kinase C, pubmed-meshheading:19006119-Receptor, Epidermal Growth Factor, pubmed-meshheading:19006119-Receptors, Interleukin-6, pubmed-meshheading:19006119-STAT Transcription Factors
pubmed:year
2009
pubmed:articleTitle
Interleukin-6 promotes 2-deoxyglucose uptake through p44/42 MAPKs activation via Ca2+/PKC and EGF receptor in primary cultured chicken hepatocytes.
pubmed:affiliation
Department of Veterinary Physiology, Biotherapy Human Resources Center (BK21), College of Veterinary Medicine, Chonnam National University, Gwangju, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't