Linked Life Data

19660180

Source:http://linkedlifedata.com/resource/pubmed/id/19660180

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-2-26
pubmed:abstractText
Adipose tissue contains a mesenchymal stem cell (MSC) population known as adipose-derived stem cells (ASCs) capable of differentiating into different cell types. Our aim was to induce hepatic transdifferentiation of ASCs by sequential exposure to several combinations of cytokines, growth factors, and hormones. The most efficient hepatogenic protocol includes fibroblastic growth factors (FGF) 2 and 4 and epidermal growth factor (EGF) (step 1), hepatocyte growth factor (HGF), FGF2, FGF4, and nicotinamide (Nic) (step 2), and oncostatin M (OSM), dexamethasone (Dex), and insulin-tranferrin-selenium (step 3). This protocol activated transcription factors [GATA6, Hex, CCAAT/enhancer binding protein alpha and beta (CEBPalpha and beta), peroxisome proliferator-activated receptor-gamma, coactivator 1 alpha (PGC1alpha), and hepatocyte nuclear factor 4 alpha (HNF4alpha)], which promoted a characteristic hepatic phenotype, as assessed by new informative markers for the step-by-step hepatic transdifferentiation of hMSC [early markers: albumin (ALB), alpha-2-macroglobuline (alpha2M), complement protein C3 (C3), and selenoprotein P1 (SEPP1); late markers: cytochrome P450 3A4 (CYP3A4), apolipoprotein E (APOE), acyl-CoA synthetase long-chain family member 1 (ACSL1), and angiotensin II receptor, type 1 (AGTR1)]. The loss of adipose adult stem cell phenotype was detected by losing expression of Thy1 and inhibitor of DNA binding 3 (Id3). The reexpression of phosphoenolpyruvate corboxykinase (PEPCK), apolipoprotein C3 (APOCIII), aldolase B (ALDOB), and cytochrome P450 1A2 (CYP1A2) was achieved by transduction with a recombinant adenovirus for HNF4alpha and finally hepatic functionality was also assessed by analyzing specific biochemical markers. We conclude that ASCs could represent an alternative tool in clinical therapy for liver dysfunction and regenerative medicine.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1555-3892
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1319-40
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19660180-Adipose Tissue, pubmed-meshheading:19660180-Cell Transdifferentiation, pubmed-meshheading:19660180-Cells, Cultured, pubmed-meshheading:19660180-Dexamethasone, pubmed-meshheading:19660180-Fibroblast Growth Factors, pubmed-meshheading:19660180-Flow Cytometry, pubmed-meshheading:19660180-Gene Expression Profiling, pubmed-meshheading:19660180-Hep G2 Cells, pubmed-meshheading:19660180-Hepatocyte Growth Factor, pubmed-meshheading:19660180-Hepatocyte Nuclear Factor 4, pubmed-meshheading:19660180-Hepatocytes, pubmed-meshheading:19660180-Humans, pubmed-meshheading:19660180-Insulin, pubmed-meshheading:19660180-Mesenchymal Stem Cells, pubmed-meshheading:19660180-Niacinamide, pubmed-meshheading:19660180-Oncostatin M, pubmed-meshheading:19660180-Selenium, pubmed-meshheading:19660180-Signal Transduction, pubmed-meshheading:19660180-Transcription Factors, pubmed-meshheading:19660180-Transferrin
pubmed:year
2009
pubmed:articleTitle
Sequential hepatogenic transdifferentiation of adipose tissue-derived stem cells: relevance of different extracellular signaling molecules, transcription factors involved, and expression of new key marker genes.
pubmed:affiliation
Unidad de Hepatología Experimental, Centro de Investigación, Hospital La Fe, Valencia, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't