An insufficient increase of cytosolic free calcium level results postovulatory aging-induced abortive spontaneous egg activation in rat

Abstract

Purpose The present study was aimed to find out whether postovulatory aging-induced abortive spontaneous egg activation (SEA) is due to insufficient increase of cytosolic free Ca 2+ level. Methods Immature female rats (22-24 days old) were subjected to superovulation induction protocol. Eggs were collected 14, 17 and 19 h post-hCG surge to induce in vivo egg aging. The eggs were collected 14 h post-hCG surge and cultured in vitro for 3, 5 and 7 h to induce in vitro egg aging. The morphological changes, rate of abortive SEA, chromosomal status and cytosolic free Ca 2+ levels were analyzed. Results Postovulatory aging induced morphological features characteristics of abortive SEA in a time-dependent manner in vivo as well as in vitro. The extracellular Ca 2+ increased rate of abortive SEA during initial period of culture, while coaddition of a nifedipine (L-type Ca 2+ channel blocker) protected against postovulatory aging-induced abortive SEA. However, CI induced morphological features characteristics of egg activation (EA) in a dose-dependent manner. As compare to control, an increase of cytosolic free Ca 2+ level (1.42 times) induced abortive SEA, while further increase of cytosolic free Ca 2+ level (2.55 times) induced EA. Conclusion Our results show that an insufficient cytosolic free Ca 2+ level is associated with postovulatory aginginduced abortive SEA, while furthermore increase is required to induce EA in rat.

Calcium Signaling During Meiotic Cell Cycle Regulation and Apoptosis in Mammalian Oocytes

“…However, in some mammalian species, if fertilization does not occur, postovulatory oocyte aging mediates spontaneous exit from M‐II arrest by inducing the initiation of extrusion of second polar body (PB‐II) (Premkumar and Chaube, , ). The PB‐II does not get completely extruded and ovulated oocytes are further arrested at metaphase‐III (M‐III) like stage without forming pronuclei (Chebotareva et al, ; Premkumar and Chaube, , ; Prasad et al, ,, ,).…”

“…Growing body of evidences suggest that Ca ++ modulates oocyte physiology depending upon its intracellular Ca ++ ([Ca ++ ]i) concentration (Homa, ; Tosti, ; Whitaker, ; Naik and Pardasani, ). For instance, a transient increase of [Ca ++ ]i under physiological range triggers spontaneous exit from diplotene arrest (Fan et al, ; Chaube et al, ; Pandey et al, ) as well as M‐II arrest (Vincent et al, ; Ruddock et al, ; Lu et al, ; Chaube et al, ; Premkumar and Chaube, , ). The sustained high level beyond physiological range results in meiotic cell cycle arrest and then apoptosis (Homa et al, ; Berridge et al, ; Tripathi et al, , , , , ; Zhang and Fissore, ; Tiwari et al, ).…”

Involvement of Cyclin-Dependent Kinase 1 during Postovulatory Aging-Mediated Abortive Spontaneous Egg Activation in Rat Eggs CulturedIn Vitro

“…Fertilizing spermatozoa trigger the egg activation process, which is characterized by meiotic resumption from MII arrest, corticle granule exocytosis, pronuclei formation, and complete extrusion of the second polar body (PBII) (Premkumar and Chaube, 2013;Xu et al, 1997). However, in a few mammalian species, ovulated eggs do not wait for fertilization and quickly undergo postovulatory aging-mediated spontaneous exit from MII arrest and initiation of extrusion of PBII; however, it never gets completely extruded, so-called abortive spontaneous egg activation (SEA) (Chebotareva et al, 2011;Chaube, 2013, 2014).…”

“…Few studies suggest that insufficient release of calcium (Ca 2+ ) from internal stores, like the endoplasmic reticulum (ER), through ryanodine receptor (RyR) channels thereby increases cytosolicfree Ca 2+ and is involved during postovulatory aging-mediated abortive SEA (Premkumar and Chaube, 2013, 2015.…”

“…Cyclin B1 degradation as well as inactivation of MAD2 result in meiotic exit from diplotene arrest and progression to the MII stage (Homer et al, 2005;Zhang et al, 2004). Although MPF destabilization/stabilization plays a major role in meiotic exit from MII arrest (Oh et al, 2011(Oh et al, , 2013Premkumar and Chaube, 2013, 2015, studies suggest that specific phosphorylation of Cdk1 and involvement of Cdk1 activity associate with meiotic resumption from diplotene arrest (Davydenko et al, 2013;Jang et al, 2014;Pandey et al, 2014). However, it remains unclear whether the specific phosphorylation status of Cdk1 as well as cyclin B1 level and Cdk1 activity are involved during postovulatory agingmediated abortive SEA.…”