Effects of carbonic anhydrase-related protein VIII on human cells harbouring an A8344G mitochondrial DNA mutation
Tze-Kai Wang1, Che-Kun Cheng1, Tang-Hao Chi1
1*Department of Life Science, Tunghai University, Taichung, Taiwan, Republic of China.
Abstract:
MERRF (myoclonus epilepsy associated with ragged-red fibres) is a maternally inherited mitochondrial encephalomyopathy with various syndromes involving both muscular and nervous systems. The most common mutation in MERRF syndrome, the A8344G mutation in mtDNA, has been associated with severe defects in the respiratory function of mitochondria. In the present study, we show that there is a significant decrease in CA8 (carbonic anhydrase-related protein VIII) in cybrids harbouring the MERRF A8344G mutation. CA8 deficiency and mutations were found to be associated with a distinctive lifelong gait disorder in wdl (Waddles) mice and novel syndromes characterized by cerebellar ataxia and mental retardation in humans. The results of the present study showed that overexpression of CA8 in MERRF cybrids significantly decreased cell death induced by STS (staurosporine) treatment, suggesting a protective function of CA8 in cells harbouring the A8344G mutation of mtDNA. Interestingly, an increase in the formation of LC3-II (microtubule-associated protein 1 light chain 3-II) was found in the cybrids with down-regulated CA8 expression, suggesting that reduced expression of CA8 leads to autophagy activation. Furthermore, cybrids exhibiting down-regulated CA8 showed increased cytosolic Ca2+ signals and reduced levels of phospho-Akt compared with those in the cybrids with overexpressed CA8, indicating that phospho-Akt is involved in the protection of cells by CA8. Our findings suggest that CA8 is involved in the autophagic pathway and may have a protective role in cultured cells from patients with MERRF. Targeting CA8 and the downstream autophagic pathway might help develop therapeutic agents for treatment of MERRF syndrome in the future.
Insights
Carbonic anhydrase-related protein VIII (CA8) is decreased in MERRF syndrome, a mitochondrial disorder. CA8 protects cells and may offer a therapeutic target for MERRF syndrome.
Area of Science:
- Neuroscience
- Genetics
- Cell Biology
Background:
- MERRF (myoclonus epilepsy associated with ragged-red fibres) is a maternally inherited mitochondrial encephalomyopathy.
- The common A8344G mutation in mtDNA causes severe mitochondrial respiratory defects in MERRF syndrome.
Purpose of the Study:
- To investigate the role of carbonic anhydrase-related protein VIII (CA8) in MERRF syndrome.
- To explore the potential of CA8 as a therapeutic target for MERRF syndrome.
Main Methods:
- Studied CA8 levels in cybrids with the MERRF A8344G mutation.
- Examined the effects of CA8 overexpression and deficiency on cell death, autophagy (LC3-II formation), cytosolic Ca2+ signals, and phospho-Akt levels.
- Correlated CA8 deficiency with gait disorders in Waddles mice and neurological symptoms in humans.
Main Results:
- CA8 levels were significantly decreased in MERRF cybrids.
- CA8 overexpression protected MERRF cybrids from staurosporine-induced cell death.
- Reduced CA8 expression led to increased autophagy (LC3-II), elevated cytosolic Ca2+, and decreased phospho-Akt.
Conclusions:
- CA8 plays a protective role in cells with the MERRF A8344G mutation.
- CA8 is involved in the autophagic pathway and influences phospho-Akt signaling.
- Targeting CA8 and the autophagic pathway may offer new therapeutic strategies for MERRF syndrome.
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