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The Src family kinases contribute to MII arrest maintenance in aging porcine oocytes

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60460709%3A41210%2F25%3A102382" target="_blank" >RIV/60460709:41210/25:102382 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00027014:_____/25:10006344

  • Výsledek na webu

    <a href="https://doi.org/10.1016/j.theriogenology.2025.117614" target="_blank" >https://doi.org/10.1016/j.theriogenology.2025.117614</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.theriogenology.2025.117614" target="_blank" >10.1016/j.theriogenology.2025.117614</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    The Src family kinases contribute to MII arrest maintenance in aging porcine oocytes

  • Popis výsledku v původním jazyce

    Mature mammalian oocytes arrest meiosis in metaphase II (MII). If the oocyte is not fertilized, it can spontaneously break the MII arrest. Spontaneous activation and postovulatory aging hinder precisely timed and regulated embryonic development. To elucidate the role of Src family protein tyrosine kinases (SFKs) in porcine oocyte MII arrest, activation, and aging, we used a specific SFK inhibitor and immunolocalization. The 24h-prolonged oocyte culture in the presence of SFK inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine (PP2) increased (P < 0.05) the proportion of spontaneously activated porcine oocytes compared to controls. Further culture with PP2 inhibitor led to an increase (P < 0.05) in the parthenogenetic embryos and a decrease (P <0.05) in lytic oocytes. SFK inhibition did not affect (P > 0.05) the proportion of ionophore A23187activated oocytes. SFKs were localized in the perichromosomal region, in the pronuclei, in the cytoplasm, and on the plasma membrane of oocytes and parthenogenetic embryos after 24, 48, and 72 h of prolonged in vitro culture. The greatest SFKs fluorescence was detected after a 24h-prolonged culture on the plasma membrane of MII oocytes. In embryos and fragmented oocytes, intense fluorescence was detected in the cleavage furrow region and on the membrane of apoptotic vesicles, respectively. Our results reveal the involvement of SFKs in MII arrest maintenance, though they don't appear to modulate the early processes of ionophore-stimulated parthenogenetic activation. Changes in the distribution of SFKs during prolonged culture suggest their role in signaling cascades associated with actin filament cytoskeleton organization.

  • Název v anglickém jazyce

    The Src family kinases contribute to MII arrest maintenance in aging porcine oocytes

  • Popis výsledku anglicky

    Mature mammalian oocytes arrest meiosis in metaphase II (MII). If the oocyte is not fertilized, it can spontaneously break the MII arrest. Spontaneous activation and postovulatory aging hinder precisely timed and regulated embryonic development. To elucidate the role of Src family protein tyrosine kinases (SFKs) in porcine oocyte MII arrest, activation, and aging, we used a specific SFK inhibitor and immunolocalization. The 24h-prolonged oocyte culture in the presence of SFK inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine (PP2) increased (P < 0.05) the proportion of spontaneously activated porcine oocytes compared to controls. Further culture with PP2 inhibitor led to an increase (P < 0.05) in the parthenogenetic embryos and a decrease (P <0.05) in lytic oocytes. SFK inhibition did not affect (P > 0.05) the proportion of ionophore A23187activated oocytes. SFKs were localized in the perichromosomal region, in the pronuclei, in the cytoplasm, and on the plasma membrane of oocytes and parthenogenetic embryos after 24, 48, and 72 h of prolonged in vitro culture. The greatest SFKs fluorescence was detected after a 24h-prolonged culture on the plasma membrane of MII oocytes. In embryos and fragmented oocytes, intense fluorescence was detected in the cleavage furrow region and on the membrane of apoptotic vesicles, respectively. Our results reveal the involvement of SFKs in MII arrest maintenance, though they don't appear to modulate the early processes of ionophore-stimulated parthenogenetic activation. Changes in the distribution of SFKs during prolonged culture suggest their role in signaling cascades associated with actin filament cytoskeleton organization.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    40301 - Veterinary science

Návaznosti výsledku

  • Projekt

    Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach

Ostatní

  • Rok uplatnění

    2025

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    Theriogenology

  • ISSN

    0093-691X

  • e-ISSN

    1879-3231

  • Svazek periodika

    248

  • Číslo periodika v rámci svazku

    neuvedeno

  • Stát vydavatele periodika

    GB - Spojené království Velké Británie a Severního Irska

  • Počet stran výsledku

    10

  • Strana od-do

  • Kód UT WoS článku

    001545893600001

  • EID výsledku v databázi Scopus

    2-s2.0-105012131274