Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/1179
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dc.contributor.authorPetrović, Vesnaen_US
dc.contributor.authorBuzadžić, Biljanaen_US
dc.contributor.authorKorać, Aleksandraen_US
dc.contributor.authorVasilijević, Anaen_US
dc.contributor.authorJanković, Aleksandraen_US
dc.contributor.authorKorać, Batoen_US
dc.date.accessioned2019-08-16T12:52:56Z-
dc.date.available2019-08-16T12:52:56Z-
dc.date.issued2010-08-01-
dc.identifier.issn1532-0456-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/1179-
dc.description.abstractMolecular mechanisms underlying interscapular brown adipose tissue (IBAT) thermogenesis were elucidated. Namely, gene and/or protein expression of uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor γ (PPARγ), PPARγ-coactivator-1α (PGC-1α), vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) - key molecules that regulate thermogenesis-related processes - mitochondriogenesis, angiogenesis and IBAT hyperplasia, in rats subjected to cold (4 ± 1 °C) for 1, 3, 7, 12, 21 and 45 days were investigated. Particularly, to examine influence of nitric oxide (NO) on IBAT thermogenic-program, cold-exposed animals were treated by l-arginine or Nω-nitro-l-arginine-methyl ester (L-NAME). Related to control (22 ± 1 °C), cold induced time-coordinated UCP1, PPARγ and PGC-1α transcriptional activation accompanied by PCNA activation and increased VEGF immunolabeling that correlate with endothelial NO synthase (eNOS) transcriptional activation suggesting NO involvement in these thermogenic-factors activation. Observed molecular changes were translated into increased mitochondrial-remodeling, angiogenesis, and IBAT hyperplasia. l-Arginine augmented and prolonged cold-induced increase of eNOS, inducible NOS and thermogenic-molecules expression, IBAT nerve supply, vascularity, hyperplasia and mitochondrial-remodeling, while L-NAME had an opposite effects. Results show that NO improves thermogenesis-related mitochondriogenesis, angiogenesis and tissue hyperplasia, positively affecting molecular basis of these processes, suggesting that NO is an essential regulator of IBAT thermogenic-program operating, at genes, proteins and tissue structure levels. © 2010 Elsevier Inc. All rights reserved.en_US
dc.language.isoenen_US
dc.relationMinistry of Science and Technological Development of the Republic of Serbia [143050]en_US
dc.relationCOST FA0602 Actionen_US
dc.relation.ispartofComparative Biochemistry and Physiology - C Toxicology and Pharmacologyen_US
dc.subjectBrown adipose tissueen_US
dc.subjectColden_US
dc.subjectNitric oxideen_US
dc.subjectColden_US
dc.subjectNitric oxideen_US
dc.subjectPGC-1αen_US
dc.subjectPPARγen_US
dc.subjectUCP1en_US
dc.titleNO modulates the molecular basis of rat interscapular brown adipose tissue thermogenesisen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.cbpc.2010.03.008-
dc.identifier.pmid20363363-
dc.identifier.scopus2-s2.0-77952892288-
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/77952892288-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of Cell and Tissue Biology-
crisitem.author.orcid0000-0002-3044-9963-
crisitem.author.orcid0000-0001-5272-579X-
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