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

Abstract

Calcium (Ca++ ) is one of the major signal molecules that regulate various aspects of cell functions including cell cycle progression, arrest, and apoptosis in wide variety of cells. This review summarizes current knowledge on the differential roles of Ca++ in meiotic cell cycle resumption, arrest, and apoptosis in mammalian oocytes. Release of Ca++ from internal stores and/or Ca++ influx from extracellular medium causes moderate increase of intracellular Ca++ ([Ca++ ]i) level and reactive oxygen species (ROS). Increase of Ca++ as well as ROS levels under physiological range trigger maturation promoting factor (MPF) destabilization, thereby meiotic resumption from diplotene as well as metaphase-II (M-II) arrest in oocytes. A sustained increase of [Ca++ ]i level beyond physiological range induces generation of ROS sufficient enough to cause oxidative stress (OS) in aging oocytes. The increased [Ca++ ]i triggers Fas ligand-mediated oocyte apoptosis. Further, OS triggers mitochondria-mediated oocyte apoptosis in several mammalian species. Thus, Ca++ exerts differential roles on oocyte physiology depending upon its intracellular concentration. A moderate increase of [Ca++ ]i as well as ROS mediate spontaneous resumption of meiosis from diplotene as well as M-II arrest, while their high levels cause meiotic cell cycle arrest and apoptosis by operating both mitochondria- as well as Fas ligand-mediated apoptotic pathways. Indeed, Ca++ regulates cellular physiology by modulating meiotic cell cycle and apoptosis in mammalian oocytes. J. Cell. Physiol. 232: 976-981, 2017. © 2016 Wiley Periodicals, Inc.