ABSTRACT
Mitochondrion is an organelle containing its own genome in eukaryotic cells , which encodes 37 genes involved in mitochondrial functions .Mitoepigenetic regulation is a major form of mitochondrial genome-encoded genes that regulates the expression levels without altering the sequences of the genes .The mitoepigenetic regulation is involved in the occurrence and development of various diseases .This paper reviews the progress of mitoepigenetic regulation and Alzhe-imer disease.
ABSTRACT
Mitochondrion is an organelle containing its own genome in eukaryotic cells , which encodes 37 genes involved in mitochondrial functions .Mitoepigenetic regulation is a major form of mitochondrial genome-encoded genes that regulates the expression levels without altering the sequences of the genes .The mitoepigenetic regulation is involved in the occurrence and development of various diseases .This paper reviews the progress of mitoepigenetic regulation and Alzhe-imer disease.
ABSTRACT
AIM:To investigate the effect of over-expression of peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α) on mitochondrial morphology and cell apoptosis in the cortical neurons with oxygen glucose depriva-tion/reoxygenation(OGD/R). METHODS:The whole gene sequence of PGC-1α was obtained from the cerebral cortex of C57BL/6 mice by RT-PCR and cloned into the eukaryotic expression vector pEGFP-N1. The pEGFP-N1-PGC-1α was iden-tified by PCR,and transfected into cortical neurons. The level of PGC-1α expression was identified by Western blot. The cortical neurons transfected with pEGFP-N1 and pEGFP-N1-PGC-1α vectors were treated with OGD/R. The mitochondrial mass,reactive oxygen species (ROS) and ATP production,cell apoptosis and changes of cleaved caspase-3 were detected by MitoTracker Red staining,flow cytometry,ATP metabolic assay kit and TUNEL. RESULTS:Over-expression of PGC-1α inhibited the decrease in mitochondrial biogenesis capacity and the ROS formation of OGD/R neurons(P<0.05),en-hanced the ability of ATP synthesis (P<0.01),inhibited neuronal apoptosis (P<0.01) and decreased the activation of caspase-3 (P<0.01). CONCLUSION:PGC-1α over-expression inhibits neuronal apoptosis with OGD/R treatment by promoting mitochondrial biogenesis,inhibiting the production of ROS and maintaining mitochondrial function. PGC-1α may be used as a target for the development of cerebral ischemia/reperfusion injury drugs.