NO modulates the molecular basis of rat interscapular brown adipose tissue thermogenesis

Autor: Aleksandra Korac, V.M. Petrović, Aleksandra Jankovic, Biljana Buzadžić, Ana Vasilijević, Bato Korac
Rok vydání: 2010
Předmět:
Male
medicine.medical_specialty
Nitric Oxide Synthase Type III
Arginine
Physiology
Angiogenesis
Health
Toxicology and Mutagenesis
Nitric Oxide Synthase Type II
Biology
Nitric Oxide
Toxicology
Biochemistry
Ion Channels
Nitric oxide
Mitochondrial Proteins
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Adipose Tissue
Brown
Enos
Internal medicine
Brown adipose tissue
medicine
Animals
Peripheral Nerves
RNA
Messenger
Uncoupling Protein 1
030304 developmental biology
0303 health sciences
RNA-Binding Proteins
Thermogenesis
Cell Biology
General Medicine
biology.organism_classification
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Thermogenin
Rats
PPAR gamma
Vascular endothelial growth factor
NG-Nitroarginine Methyl Ester
Endocrinology
medicine.anatomical_structure
chemistry
030220 oncology & carcinogenesis
Transcription Factors
Zdroj: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology. 152:147-159
ISSN: 1532-0456
DOI: 10.1016/j.cbpc.2010.03.008
Popis: 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 gamma (PPARgamma), PPARgamma-coactivator-1alpha (PGC-1alpha), 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 degrees C) for 1, 3, 7, 12, 21 and 45days were investigated. Particularly, to examine influence of nitric oxide (NO) on IBAT thermogenic-program, cold-exposed animals were treated by l-arginine or N(omega)-nitro-l-arginine-methyl ester (L-NAME). Related to control (22+/-1 degrees C), cold induced time-coordinated UCP1, PPARgamma and PGC-1alpha 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.
Databáze: OpenAIRE
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