Linked Life Data

19784879

Source:http://linkedlifedata.com/resource/pubmed/id/19784879

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-1-21
pubmed:abstractText
Transforming growth factor (TGF) beta1 has been shown to promote differentiation of smooth muscle cells (SMC) from some precursor cells. Whether endogenous TGF beta1 also contributes to SMC differentiation during embryogenesis, however, remains unclear. In this study, a plasmid-based TGF beta1 RNA interference embryonic stem (ES) cell line was constructed. Morphological observation showed that TGF beta1 knockdown significantly prevented differentiated cells from outgrowing from ES cells-derived embryoid bodies (EBs). Immunofluorescence staining indicated that SM alpha-actin-positive cells were confluent and dense in the control group but dispersed in the TGF beta1 knockdown group. RT-PCR and western blot suggested that TGF beta1 knockdown resulted in a decrease in the expression of early SMC markers SM alpha-actin and myocardin in EBs. Both the retarded extension of cell outgrowth and the decrease in SM alpha-actin and myocardin expression could not be rescued by addition of exogenous TGF beta1. These data suggest that endogenous TGF beta1 promotes differentiation of SMC from ES cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1880-6562
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-41
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Endogenous transforming growth factor (TGF) beta1 promotes differentiation of smooth muscle cells from embryonic stem cells: stable plasmid-based siRNA silencing of TGF beta1 gene expression.
pubmed:affiliation
Department of Cardiology, Cardiovascular Research Institute, Shenyang Northern Hospital, 110016 Shenyang, Liaoning, China. han_yaling@yahoo.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't