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Daxx inhibits stress-induced apoptosis in cardiac myocytes
Renata Zobalova1, Emma Swettenham, Jaromira Chladova
1Apoptosis Research Group, School of Medical Science, Griffith University and Griffith Institute of Health and Medical Research, Southport, Queensland, Australia.
Abstract:
The role of the death-associated protein Daxx in modulation of apoptosis induced in cardiac myocytes by oxidative stress was studied. Exposure of cultured cardiomyocyte-like cells to oxidative stress or simulated hypoxia increased the level of accumulated ROS and apoptosis. Under conditions of sub-apoptotic stimulation of cardiac myocytes, there was no increase in the level of the Daxx protein, but it translocated from the nucleus to the cytoplasm. Daxx overexpression protected the cells from apoptosis, while they were sensitised to cell death following its down-regulation by siRNA. Moreover, lowering the level of the Daxx protein sensitised cardiac myocytes to spontaneous apoptosis, suggesting that the protein may also have a pro-survival role under physiological conditions. Finally, it was shown that DJ-1, a protein suggested previously to sequester Daxx in the nucleus under conditions of oxidative stress (thereby preventing its cytosolic translocation), was localised solely in the cytoplasm of cardiac myocytes. This indicates that the protein does not modulate the apoptosis regulatory activity of Daxx in cardiac myocytes by its nuclear sequestration. Taken together, Daxx plays a protective role in cultured cardiomyocyte-like cells, at least under the conditions used.
Insights
Death-associated protein Daxx protects cardiac cells from oxidative stress-induced apoptosis. Daxx
Area of Science:
- Cardiovascular Biology
- Cell Death Pathways
- Molecular Cardiology
Background:
- Oxidative stress is a key factor in cardiac myocyte apoptosis.
- The role of death-associated protein Daxx in cardiac cell apoptosis is not fully understood.
Purpose of the Study:
- To investigate the role of Daxx in apoptosis of cardiac myocytes induced by oxidative stress.
- To explore the interaction between Daxx, DJ-1, and apoptosis regulation in cardiomyocytes.
Main Methods:
- Cultured cardiomyocyte-like cells were exposed to oxidative stress or simulated hypoxia.
- Changes in reactive oxygen species (ROS) levels, apoptosis, and Daxx protein localization were assessed.
- Daxx protein levels were modulated using overexpression and small interfering RNA (siRNA).
Main Results:
- Oxidative stress increased ROS and apoptosis in cardiac myocytes.
- Daxx translocated from the nucleus to the cytoplasm under sub-apoptotic stimulation.
- Daxx overexpression protected cells from apoptosis, while siRNA-mediated knockdown sensitized them.
- DJ-1 protein was found in the cytoplasm, not sequestering Daxx in the nucleus.
Conclusions:
- Daxx plays a protective role against apoptosis in cardiac myocytes under studied conditions.
- Daxx's nuclear sequestration by DJ-1 does not appear to regulate its apoptotic function in these cells.
- Daxx may possess a pro-survival role in cardiac myocytes under physiological conditions.
