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  • Wiley  (3)
  • Yadav, Pramod K.  (3)
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  • Wiley  (3)
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  • 1
    In: Journal of Cellular Physiology, Wiley, Vol. 234, No. 6 ( 2019-06), p. 8019-8027
    Abstract: The maximum number of germ cells is present during the fetal life in mammals. Follicular atresia results in rapid depletion of germ cells from the cohort of the ovary. At the time of puberty, only a few hundred ( 〈 1%) germ cells are either culminated into oocytes or further get eliminated during the reproductive life. Although apoptosis plays a major role, necrosis as well as necroptosis, might also be involved in germ cell elimination from the mammalian ovary. Both necrosis and necroptosis show similar morphological features and are characterized by an increase in cell volume, cell membrane permeabilization, and rupture that lead to cellular demise. Necroptosis is initiated by tumor necrosis factor and operated through receptor interacting protein kinase as well as mixed lineage kinase domain‐like protein. The acetylcholinesterase, cytokines, starvation, and oxidative stress play important roles in necroptosis‐mediated granulosa cell death. The granulosa cell necroptosis directly or indirectly induces susceptibility toward necroptotic or apoptotic cell death in oocytes. Indeed, prevention of necrosis and necroptosis pathways using their specific inhibitors could enhance growth/differentiation factor‐9 expression, improve survivability as well as the meiotic competency of oocytes, and prevent decline of reproductive potential in several mammalian species and early onset of menopause in women. This study updates the information and focuses on the possible involvement of necrosis and necroptosis in germ cell depletion from the mammalian ovary.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2018
    In:  Journal of Cellular Physiology Vol. 233, No. 8 ( 2018-08), p. 5530-5536
    In: Journal of Cellular Physiology, Wiley, Vol. 233, No. 8 ( 2018-08), p. 5530-5536
    Abstract: In mammals, journey from metaphase‐I (M‐I) to metaphase‐II (M‐II) is important since oocyte extrude first polar body (PB‐I) and gets converted into haploid gamete. The molecular and cellular changes associated with meiotic cell cycle progression from M‐I to M‐II stage and extrusion of PB‐I remain ill understood. Several factors drive oocyte meiosis from M‐I to M‐II stage. The mitogen‐activated protein kinase3/1 (MAPK3/1), signal molecules and Rho family GTPases act through various pathways to drive cell cycle progression from M‐I to M‐II stage. The down regulation of MOS/MEK/MAPK3/1 pathway results in the activation of anaphase‐promoting complex/cyclosome (APC/C). The active APC/C destabilizes maturation promoting factor (MPF) and induces meiotic resumption. Several signal molecules such as, c‐Jun N‐terminal kinase (JNK2), SENP3, mitotic kinesin‐like protein 2 (MKlp2), regulator of G‐protein signaling (RGS2), Epsin2, polo‐like kinase 1 (Plk1) are directly or indirectly involved in chromosomal segregation. Rho family GTPase is another enzyme that along with cell division cycle (Cdc42) to form actomyosin contractile ring required for chromosomal segregation. In the presence of origin recognition complex (ORC4), eccentrically localized haploid set of chromosomes trigger cortex differentiation and determine the division site for polar body formation. The actomyosin contractile activity at the site of division plane helps to form cytokinetic furrow that results in the formation and extrusion of PB‐I. Indeed, oocyte journey from M‐I to M‐II stage is coordinated by several factors and pathways that enable oocyte to extrude PB‐I. Quality of oocyte directly impact fertilization rate, early embryonic development, and reproductive outcome in mammals.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1478143-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    In: Journal of Cellular Biochemistry, Wiley, Vol. 119, No. 1 ( 2018-01), p. 123-129
    Abstract: The oocyte quality remains as one of the major problems associated with poor in vitro fertilization (IVF) rate and assisted reproductive technology (ART) failure worldwide. The oocyte quality is dependent on its meiotic maturation that begins inside the follicular microenvironment and gets completed at the time of ovulation in most of the mammalian species. Follicular oocytes are arrested at diplotene stage of first meiotic prophase. The resumption of meiosis from diplotene arrest, progression through metaphase‐I (M‐I) and further arrest at metaphase‐II (M‐II) are important physiological requirements for the achievement of meiotic competency in mammalian oocytes. The achievement of meiotic competency is dependent upon cyclic stabilization/destabilization of maturation promoting factor (MPF). The mitogen‐activated protein kinase3/1 (MAPK3/1) modulates stabilization/destabilization of MPF in oocyte by interacting either with signal molecules, transcription and post‐transcription factors in cumulus cells or cytostatic factors (CSFs) in oocyte. MPF regulates meiotic cell cycle progression from diplotene arrest to M‐II arrest and directly impacts oocyte quality. The MAPK3/1 activity is not reported during spontaneous meiotic resumption but its activity in cumulus cells is required for gonadotropin‐induced oocyte meiotic resumption. Although high MAPK3/1 activity is required for the maintenance of M‐II arrest in several mammalian species, its cross‐talk with MPF remains to be elucidated. Further studies are required to find out the MAPK3/1 activity and its impact on MPF destabilization/stabilization during achievement of meiotic competency, an important period that decides oocyte quality and directly impacts ARTs outcome in several mammalian species including human. J. Cell. Biochem. 119: 123–129, 2018. © 2017 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0730-2312 , 1097-4644
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1479976-5
    SSG: 12
    Location Call Number Limitation Availability
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