Expression of mitochondrial uncoupling protein 3 and adenine nucleotide translocase 1 genes in developing rat heart: putative involvement in control of mitochondrial membrane potential
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12676547
DOI
10.1016/s0022-2828(03)00016-6
PII: S0022282803000166
Knihovny.cz E-resources
- MeSH
- Ion Channels MeSH
- Rats MeSH
- Membrane Potentials MeSH
- Mitochondrial Proteins MeSH
- Mitochondria metabolism physiology MeSH
- Myocardium metabolism MeSH
- Animals, Newborn MeSH
- Rats, Wistar MeSH
- Receptors, Cytoplasmic and Nuclear genetics MeSH
- Heart growth & development physiology MeSH
- Transcription Factors genetics MeSH
- Adenine Nucleotide Translocator 1 genetics metabolism MeSH
- Adenine Nucleotide Translocator 2 genetics MeSH
- Carrier Proteins genetics metabolism physiology MeSH
- Uncoupling Protein 3 MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Ion Channels MeSH
- Mitochondrial Proteins MeSH
- Receptors, Cytoplasmic and Nuclear MeSH
- Transcription Factors MeSH
- Adenine Nucleotide Translocator 1 MeSH
- Adenine Nucleotide Translocator 2 MeSH
- Carrier Proteins MeSH
- Ucp3 protein, rat MeSH Browser
- Uncoupling Protein 3 MeSH
Postnatal maturation of the heart depends on the switch from glycolytic to oxidative metabolism and it is associated with decreasing tolerance to oxygen deprivation. Therefore, changes in composition and function of cardiac mitochondria during postnatal development require detailed characterization. Left-ventricular myocardium of prenatal, and 1-, 2-, 5-, 10-, 20-, 28-, 50-, 60-, and 90-d-old male Wistar rats was studied. The expression of uncoupling proteins (UCPs), adenine nucleotide translocase (ANT), and peroxisome proliferator-activated receptor alpha (PPARalpha) genes was characterized by northern blotting (UCP2), real-time quantitative RT-PCR (UCP2, UCP3, ANT1, ANT2, and PPARalpha), and by immunoblotting (UCP3). In isolated mitochondria, cytochromes a + a(3) were quantified by a spectrophotometry, and mitochondrial membrane potential (MMP) was measured using Rhodamine 123 (by spectrofluorimetry and flow cytometry). The specific content of cytochromes in mitochondria increased two-fold between birth and day 30, similarly, as the expression of ANT1 and PPARalpha genes. Postnatal activation in the expression of UCP2, UCP3, ANT1 and PPARalpha genes resulted in the expression maxima between days 20 and 30. The content/expression declined following day 20 (UCP2, UCP3, and PPARalpha) or 30 (cytochromes and ANT1), while expression of ANT2 declined continuously during the first month of life. In 1-d-old animals a single population of mitochondria with a relatively high MMP was observed; with increasing age, a second population of mitochondria with a significantly lower MMP appeared. The results support the view that mitochondrial energy conversion in heart changes during ontogeny and suggest the involvement of UCP3 and/or ANT1 in the control mechanism.
References provided by Crossref.org
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
Neonatal cardiac mitochondria and ischemia/reperfusion injury
Postnatal development of phospholipids and their fatty acid profile in rat heart
