Abstract

Sirtuins have been implicated in diverse biological processes, including oxidative stress, energy metabolism, cell migration, and aging. Here, we employed Sirtuin inhibitors, nicotinamide (NAM) and Sirtinol, to investigate their effects on porcine oocyte maturation respectively. The rate of polar body extrusion in porcine oocytes decreased after treatment with NAM and Sirtinol, accompanied with the failure of cumulus cell expansion. We further found that NAM and Sirtinol significantly disrupted oocyte polarity, and inhibited the formation of actin cap and cortical granule-free domain (CGFD). Moreover, the abnormal spindles and misaligned chromosomes were readily detected during porcine oocyte maturation after treatment with NAM and Sirtinol. Together, these results suggest that Sirtuins are involved in cortical polarity and spindle organization in porcine oocytes.

Highlights

  • Accepted: June 21, 2015Published: July 15, 2015

  • Effects of NAM and Sirtinol on meiotic maturation of porcine oocytes To investigate the possible involvement of Sirtuins in porcine oocyte meiotic maturation, Cumulus-oocyte complexes (COCs) were treated with two kinds of Sirtuin inhibitors: NAM and Sirtinol

  • The results indicated that NAM and Sirtinol treatment reduced the rate of polar body extrusionand disrupted actin assembly in porcine oocytes

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Summary

Introduction

Oocyte maturation involves two aspects, cytoplasmic and nuclear maturation Both steps are essential for the formation of a fertilizable egg that can subsequently develop into a live offspring. Oocyte maturation is a complex biological process, and development of oocyte polarity involves the assembly of actin and CGs. Sirtuins are nicotinamide adenine dinucleotide (NAD)-dependent deacetylases that are highly conserved from bacteria to humans. We investigated the effects of inhibition of Sirtuin activity on porcine oocyte maturation using two specific inhibitors, NAM and Sirtinol. Treatment with these inhibitors reduced the rate of polar body extrusion and disrupted actin distribution and formation of cortical granulefree domain (CGFD). Inhibition of Sirtuin activity led to spindle defects and chromosome misalignment in porcine oocytes

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