RyR channel-mediated increase of cytosolic free calcium level signals cyclin B1 degradation during abortive spontaneous egg activation in rat.
In few mammalian species including rat, post-ovulatory aging induces abortive spontaneous egg activation (SEA), which is morphologically characterized by exit from metaphase-II (M-II) arrest. A possibility exists that the RyR channel-mediated insufficient increase of cytosolic free Ca(2+) level could be one of the causes for post-ovulatory aging-induced abortive SEA. To test this possibility, eggs collected after 17 h post-hCG surge were cultured with or without various concentrations of nifedipine (NF), ruthenium red (RR), and KN-93 for 3 h in vitro. Morphological changes characteristic of abortive SEA, cytosolic free Ca(2+) level, cyclin B1 level, and meiotic status were analyzed. Data of the present study indicate that NF and RR inhibited post-ovulatory aging-induced abortive SEA in a concentration-dependent manner. Further, RR protected against RyR channel as well as caffeine-mediated increase of cytosolic free Ca(2+) level. In addition, KN-93 inhibited post-ovulatory aging-induced abortive SEA in a concentration-dependent manner. An increase of cytosolic free Ca(2+) level was associated with a reduction of cyclin B1 level during post-ovulatory aging-induced abortive SEA. These data indirectly suggest the involvement of RyR channels in the increase of cytosolic free Ca(2+) level. The increased cytosolic free Ca(2+) level triggers cyclin B1 degradation possibly through CaMK-II activity during post-ovulatory aging-induced abortive SEA in rat eggs cultured in vitro.
Cell Physiology Laboratory, Department of Zoology, Banaras Hindu University, Varanasi, 221005, India.
Karuppanan V
KV
Premkumar
Shail K
SK
Chaube
D000704:Analysis of Variance; D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D016922:Cellular Senescence / Q000502:physiology*; D056744:Cyclin B1 / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism*; D005455:Fluorescent Antibody Technique; D008677:Metaphase / Q000187:drug effects / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D010063:Ovum / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D059748:Proteolysis; D051381:Rats; D012430:Ruthenium Red / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology; D000096926:Benzenesulfonamides
D001596:Benzylamines; D002118:Calcium; D056744:Cyclin B1; D009543:Nifedipine; D012430:Ruthenium Red; D019837:Ryanodine Receptor Calcium Release Channel; D013449:Sulfonamides; C534701:Ccnb1 protein, rat; C072105:KN 93; D000096926:Benzenesulfonamides