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Nicotinamide: a class III HDACi delays in vitro aging of mouse oocytes
Ah Reum Lee1, Satoshi Kishigami, Tomoko Amano
1Division of Biological Science, Graduate School of Biology-Oriented Science and Technology, Kinki University, Wakayama 649-6493, Japan.
Abstract:
Postovulatory mammalian oocyte developmental potential decreases with aging in vivo and in vitro. Aging oocytes typically show cellular fragmentation and chromosome scattering with an abnormally shaped spindle over time. Previously, it was shown that histone acetylation in the mouse oocyte increased during aging and that treatment with trichostatin A (TSA), an inhibitor for class I and II histone deacetylases (HDACs), enhanced the acetylation, that is, aging. In this study, we examined the effect of nicotinamide (NAM), an inhibitor for class III HDACs, on in vitro aging of mouse oocytes as well as TSA. We found that treatment with NAM significantly inhibited cellular fragmentation, spindle elongation and astral microtubules up to 48 h of culture. Although presence of TSA partially inhibited cellular fragmentation and spindle elongation up to 36 h of culture, treatment with TSA induced chromosome scattering at 24 h of culture and more severe cellular fragmentation at 48 h of culture. Further, we found that α-tubulin, a nonhistone protein, increased acetylation during aging, suggesting that not only histone but nonhistone protein acetylation may also increase with oocyte aging. Thus, these data indicate that protein acetylation is abnormally regulated in aging oocytes, which are associated with a variety of aging phenotypes, and that class I/II and class III HDACs may play distinct roles in aging oocytes.
Insights
Nicotinamide (NAM), a class III histone deacetylase (HDAC) inhibitor, improved mouse oocyte quality during aging. Unlike trichostatin A (TSA), NAM prevented cellular fragmentation and spindle defects, suggesting distinct HDAC roles in oocyte aging.
Area of Science:
- Reproductive Biology
- Cellular Aging
- Epigenetics
Background:
- Oocyte developmental potential declines with aging, characterized by cellular fragmentation and spindle abnormalities.
- Histone acetylation increases in aging oocytes, and trichostatin A (TSA), a class I/II histone deacetylase (HDAC) inhibitor, exacerbates this.
- The role of class III HDACs in oocyte aging remains largely unexplored.
Purpose of the Study:
- To investigate the effects of nicotinamide (NAM), a class III HDAC inhibitor, on in vitro aging of mouse oocytes.
- To compare the effects of NAM with TSA on aging oocyte phenotypes.
Main Methods:
- In vitro culture of mouse oocytes to induce aging.
- Treatment with NAM (class III HDAC inhibitor) and TSA (class I/II HDAC inhibitor).
- Assessment of cellular fragmentation, spindle morphology, chromosome scattering, and α-tubulin acetylation.
Main Results:
- NAM treatment significantly inhibited cellular fragmentation and spindle/astral microtubule abnormalities up to 48 hours.
- TSA partially inhibited fragmentation and spindle elongation but induced chromosome scattering and severe fragmentation by 48 hours.
- Increased α-tubulin acetylation was observed in aging oocytes, indicating non-histone protein acetylation changes.
Conclusions:
- Protein acetylation is abnormally regulated in aging oocytes, contributing to aging phenotypes.
- Class III HDACs (inhibited by NAM) play a distinct and potentially protective role in mitigating oocyte aging.
- Class I/II HDACs (inhibited by TSA) may have detrimental effects on oocyte aging, unlike class III HDACs.
