| Literature DB >> 24316184 |
Pronrumpa Ngamsiri1, Piyajit Watcharasit2, Jutamaad Satayavivad3.
Abstract
Mitochondrial biogenesis, a mitochondrial growth and division process, is crucial for adaptation to metabolic stress. The present study demonstrated that treatment with a specific inhibitor of GSK3, SB216763, attenuated induction of mitochondrial biogenesis by a glycolysis inhibitor, 2-deoxyglucose (2-DG), without affecting this biogenesis at basal condition. Additionally, overexpression of WT-GSK3β promoted whereas GSK3β-KD attenuated 2-DG-induced mitochondrial protein expression. The mitochondrial biogenesis attenuation by GSK3 inhibitor was not due to inhibition of protein degradation. Furthermore, GSK3 inhibition further reduced transcription of mitochondrial (COXII), but not nuclear (VDAC) gene by 2-DG suggesting its participation in 2-DG-induced mitochondrial transcription. Together, our results show that GSK3 regulates mitochondrial biogenesis induced by glycolysis inhibition.Entities:
Keywords: 2-DG; 2-Deoxyglucose; AMP-activated protein kinase; AMPK; GAPDH; GSK3; GSK3β-KD; Glyceraldehyde-3-phosphate dehydrogenase; Glycogen synthase kinase-3; Glycogen synthase kinase-3 (α/β); Glycogen synthase kinase-3β-kinase dead; Mitochondrial biogenesis; Mitochondrial cytochrome b; Mitochondrial cytochrome c oxidase subunit II; Mitochondrial cytochrome c oxidase subunit III; Mitochondrial transcription factor A; NRF-1; Nuclear respiratory factor 1; PGC-1α; Peroxisome proliferator-activated receptor gamma coactivator 1α; TFAM; TK2; Thymidine kinase 2; VDAC; Voltage-dependent anion-selective channel; WT-GSK3β; Wild-type-glycogen synthase kinase-3β; mtCOXII; mtCOXIII; mtCYTB
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Year: 2013 PMID： 24316184 DOI： 10.1016/j.mito.2013.11.003
Source DB: PubMed Journal: Mitochondrion ISSN： 1567-7249 Impact factor: 4.160