Mitochondria alter morphology between an elongated and fragmented phenotype by the processes of fusion and fission and these changes correlate with metabolic function in the adult heart. It is not known whether mitochondrial morphology is linked with the changing metabolic demands of the neonatal heart as it makes the transition from the environment of the womb to the outside.Methodology
We measured changes in mitochondrial morphology at the time of birth in the murine heart (2.5 and 0 days prior to birth and 0.5, 2.5, 10 days after birth) using both electron microscopy and confocal imaging of cardiomyocytes loaded with MitoTracker dye. Gene and protein expression of mitochondrial fusion and fission proteins were also assessed.Results
In both the electron microscopic heart samples and the cardiomyocytes loaded with MitoTracker dye, there was a progressive change in mitochondrial morphology from a mainly fragmented to elongated phenotype which reached a plateau at 2.5 days after birth. Interestingly, this change in mitochondrial morphology corresponded to a significant increase in protein and gene expression of the fusion proteins Mfn1, Mfn2 and Opa1 at both 2.5 and 10 days after birth. Expression of the fission proteins Fis1 and Drp-1 remained constant.Conclusions
At the time of birth there is a change in mitochondrial morphology from a predominantly fragmented to elongated phenotype in the neonatal heart associated with augmented expression of the mitochondrial fusion genes and proteins. We are now investigating whether this change in mitochondrial morphology is required for the changing metabolic demands required at the time of birth.