Please use this identifier to cite or link to this item:
https://biore.bio.bg.ac.rs/handle/123456789/1179
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Petrović, Vesna | en_US |
dc.contributor.author | Buzadžić, Biljana | en_US |
dc.contributor.author | Korać, Aleksandra | en_US |
dc.contributor.author | Vasilijević, Ana | en_US |
dc.contributor.author | Janković, Aleksandra | en_US |
dc.contributor.author | Korać, Bato | en_US |
dc.date.accessioned | 2019-08-16T12:52:56Z | - |
dc.date.available | 2019-08-16T12:52:56Z | - |
dc.date.issued | 2010-08-01 | - |
dc.identifier.issn | 1532-0456 | - |
dc.identifier.uri | https://biore.bio.bg.ac.rs/handle/123456789/1179 | - |
dc.description.abstract | Molecular 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.iso | en | en_US |
dc.relation | Ministry of Science and Technological Development of the Republic of Serbia [143050] | en_US |
dc.relation | COST FA0602 Action | en_US |
dc.relation.ispartof | Comparative Biochemistry and Physiology - C Toxicology and Pharmacology | en_US |
dc.subject | Brown adipose tissue | en_US |
dc.subject | Cold | en_US |
dc.subject | Nitric oxide | en_US |
dc.subject | Cold | en_US |
dc.subject | Nitric oxide | en_US |
dc.subject | PGC-1α | en_US |
dc.subject | PPARγ | en_US |
dc.subject | UCP1 | en_US |
dc.title | NO modulates the molecular basis of rat interscapular brown adipose tissue thermogenesis | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1016/j.cbpc.2010.03.008 | - |
dc.identifier.pmid | 20363363 | - |
dc.identifier.scopus | 2-s2.0-77952892288 | - |
dc.identifier.url | https://api.elsevier.com/content/abstract/scopus_id/77952892288 | - |
item.languageiso639-1 | en | - |
item.cerifentitytype | Publications | - |
item.openairetype | Article | - |
item.fulltext | No Fulltext | - |
item.grantfulltext | none | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
crisitem.author.dept | Chair of Cell and Tissue Biology | - |
crisitem.author.orcid | 0000-0002-3044-9963 | - |
crisitem.author.orcid | 0000-0001-5272-579X | - |
Appears in Collections: | Journal Article |
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