Calcium Signaling During Meiotic Cell Cycle Regulation and Apoptosis in Mammalian Oocytes. Issue 5 (20th November 2016)

• Record Type: Journal Article
• Authors: Tiwari, Meenakshi; Prasad, Shilpa; Shrivastav, Tulsidas G.; Chaube, Shail K.
• Is Part Of: Journal of cellular physiology. Volume 232:Issue 5(2017:May)
• Page Start: 976
• Page End: 981
• Publication Date: 2016-11-20
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.25670
• Languages: English
• ISSNs: 0021-9541

Abstract

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. Abstract : A moderate increase of [Ca++]i level under physiological range induces generation of ROS that result in decrease of cAMP level and increase of CaMKII activity. A decrease of intraoocyte cAMP level and increase of CaMKII activity directly and/or indirectly triggers MPF destabilization thereby meiotic resumption from diplotene as well as M‐II arrest. The high level of [Ca++]i beyond physiological range triggers Fas ligand‐mediated apoptosis and induces OS. The increased OS triggers oocyte apoptosis through mitochondria‐mediated pathway. Indeed, high level of [Ca++]i and ROS‐mediated meiotic cell cycle arrest and apoptosis could be interlinked in mammalian oocytes.