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Article: Microarray analysis suggests that burn injury results in mitochondial dysfunction in human skeletal muscle

TitleMicroarray analysis suggests that burn injury results in mitochondial dysfunction in human skeletal muscle
Authors
Issue Date2009
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htm
Citation
International Journal Of Molecular Medicine, 2009, v. 24 n. 3, p. 387-392 How to Cite?
AbstractBurn 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 PPARα, PPARγ and PPARδ also known as PPARβ or PPARβ/ δ), 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 PPARγ-1β (or PGC-1β) was downregulated (P<0.0001), while the expression of PPARδ was upregulated (P<0.001). Expression of PGC-1α, the closest homolog of PGC-1β 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.
Persistent Identifierhttp://hdl.handle.net/10722/180736
ISSN
2015 Impact Factor: 2.348
2015 SCImago Journal Rankings: 0.868
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTzika, AAen_US
dc.contributor.authorMintzopoulos, Den_US
dc.contributor.authorMindrinos, Men_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorRahme, LGen_US
dc.contributor.authorTompkins, RGen_US
dc.date.accessioned2013-01-28T01:42:07Z-
dc.date.available2013-01-28T01:42:07Z-
dc.date.issued2009en_US
dc.identifier.citationInternational Journal Of Molecular Medicine, 2009, v. 24 n. 3, p. 387-392en_US
dc.identifier.issn1107-3756en_US
dc.identifier.urihttp://hdl.handle.net/10722/180736-
dc.description.abstractBurn 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 PPARα, PPARγ and PPARδ also known as PPARβ or PPARβ/ δ), 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 PPARγ-1β (or PGC-1β) was downregulated (P<0.0001), while the expression of PPARδ was upregulated (P<0.001). Expression of PGC-1α, the closest homolog of PGC-1β 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.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htmen_US
dc.relation.ispartofInternational Journal of Molecular Medicineen_US
dc.subject.meshAdolescenten_US
dc.subject.meshBurns - Genetics - Pathologyen_US
dc.subject.meshCarrier Proteins - Genetics - Metabolismen_US
dc.subject.meshChilden_US
dc.subject.meshChild, Preschoolen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHeat-Shock Proteins - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshInfanten_US
dc.subject.meshIon Channels - Genetics - Metabolismen_US
dc.subject.meshMitochondria - Genetics - Pathologyen_US
dc.subject.meshMitochondrial Proteins - Genetics - Metabolismen_US
dc.subject.meshMuscle, Skeletal - Metabolism - Pathologyen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshPpar Alpha - Genetics - Metabolismen_US
dc.subject.meshPpar Delta - Genetics - Metabolismen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshTranscription, Geneticen_US
dc.titleMicroarray analysis suggests that burn injury results in mitochondial dysfunction in human skeletal muscleen_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.3892/ijmm_00000244en_US
dc.identifier.pmid19639232-
dc.identifier.scopuseid_2-s2.0-70349568691en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349568691&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume24en_US
dc.identifier.issue3en_US
dc.identifier.spage387en_US
dc.identifier.epage392en_US
dc.identifier.isiWOS:000268946500014-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridTzika, AA=7003635500en_US
dc.identifier.scopusauthoridMintzopoulos, D=16070342600en_US
dc.identifier.scopusauthoridMindrinos, M=6603048545en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridRahme, LG=6603919311en_US
dc.identifier.scopusauthoridTompkins, RG=7101805272en_US

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