Linked Life Data

19639232

Source:http://linkedlifedata.com/resource/pubmed/id/19639232

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-7-29
pubmed:abstractText
Burn injuries to extensive areas of the body are complicated by muscle catabolism. Elucidating the molecular mechanisms that mediate this catabolism may facilitate the development of a medical intervention. Here, we assessed the functional classification of genes that were differentially expressed in skeletal muscle following burn injury in 19 children (5.2+/-4.0 years of age), (64+/-15% total burn surface area, TBSA) relative to 13 healthy controls (11.9+/-6.0 years of age). Microarray analysis of samples taken within 10 days of burn injury revealed altered expression of a variety of genes, including some involved in cell and organelle organization and biogenesis, stress response, wound response, external stimulus response, regulation of apoptosis and intracellular signaling. The genes that encode peroxisome proliferator-activated receptors (PPARs; 3 isotypes PPARalpha, PPARgamma and PPARdelta also known as PPARbeta or PPARbeta/delta), which may serve as transcriptional nodal points and therapeutic targets for metabolic syndromes, were among those affected. In particular, expression of the main mitochondrial biogenesis factor PPARgamma-1beta (or PGC-1beta) was downregulated (P<0.0001), while the expression of PPARdelta was upregulated (P<0.001). Expression of PGC-1alpha, the closest homolog of PGC-1beta was upregulated (P=0.0037), and expression of the gene encoding mitochodrial uncoupling protein 2 (UCP2) was also upregulated (P=0.008). These results suggest that altered PPAR and mitochondrial gene expression soon after burn injury may lead to metabolic and mitochondrial dysfunction in human skeletal muscle.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1107-3756
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
387-92
pubmed:dateRevised
2011-11-3
pubmed:meshHeading
pubmed-meshheading:19639232-Adolescent, pubmed-meshheading:19639232-Burns, pubmed-meshheading:19639232-Carrier Proteins, pubmed-meshheading:19639232-Child, pubmed-meshheading:19639232-Child, Preschool, pubmed-meshheading:19639232-Gene Expression Profiling, pubmed-meshheading:19639232-Gene Expression Regulation, pubmed-meshheading:19639232-Heat-Shock Proteins, pubmed-meshheading:19639232-Humans, pubmed-meshheading:19639232-Infant, pubmed-meshheading:19639232-Ion Channels, pubmed-meshheading:19639232-Mitochondria, pubmed-meshheading:19639232-Mitochondrial Proteins, pubmed-meshheading:19639232-Muscle, Skeletal, pubmed-meshheading:19639232-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:19639232-PPAR alpha, pubmed-meshheading:19639232-PPAR delta, pubmed-meshheading:19639232-RNA, Messenger, pubmed-meshheading:19639232-Transcription, Genetic, pubmed-meshheading:19639232-Transcription Factors
pubmed:year
2009
pubmed:articleTitle
Microarray analysis suggests that burn injury results in mitochondrial dysfunction in human skeletal muscle.
pubmed:affiliation
NMR Surgical Laboratory, Department of Surgery, Massachusetts General and Shriners Hospitals, Harvard Medical School, Boston, MA 02114, USA. atzika@hms.harvard.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural