Analysis of expression profiles of genes involved in F(o)F(1)-ATP synthase biogenesis during perinatal development in rat liver and skeletal muscle
Language English Country Czech Republic Media print-electronic
Document type Comparative Study, Journal Article
PubMed
26988161
DOI
10.33549/physiolres.933126
PII: 933126
Knihovny.cz E-resources
- MeSH
- Organelle Biogenesis MeSH
- Adaptation, Physiological * MeSH
- Liver embryology growth & development metabolism MeSH
- Animals, Newborn growth & development metabolism MeSH
- Pilot Projects MeSH
- Rats, Wistar MeSH
- Proton-Translocating ATPases biosynthesis MeSH
- Gene Expression Profiling MeSH
- Muscles embryology metabolism MeSH
- Pregnancy MeSH
- Muscle Development MeSH
- Animals MeSH
- Check Tag
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
- Names of Substances
- Proton-Translocating ATPases MeSH
During the process of intra-uterine mammalian fetal development, the oxygen supply in growing fetus is low. A rapid switch from glycolysis-based metabolism to oxidative phosphorylation (OXPHOS) must proceed during early postnatal adaptation to extra-uterine conditions. Mitochondrial biogenesis and mammalian mitochondrial F(o)F(1)-ATP synthase assembly (complex V, EC 3.6.3.14, ATPase) are complex processes regulated by multiple transcription regulators and assembly factors. Using RNA expression analysis of rat liver and skeletal tissue (Rattus norvegicus, Berkenhout, 1769), we describe the expression profiles of 20 genes involved in mitochondrial maturation and ATP synthase biogenesis in detail between the 16th and 22nd day of gestation and the first 4 days of life. We observed that the most important expression shift occurred in the liver between the 20th and 22nd day of gestation, indicating that the fetus prepares for birth about two days before parturition. The detailed mechanism regulating the perinatal adaptation process is not yet known. Deeper insights in perinatal physiological development will help to assess mitochondrial dysfunction in the broader context of cell metabolism in preterm newborns or neonates with poor adaptation to extra-uterine life.
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