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Divalent cation influx and calcium homeostasis in germinal vesicle mouse oocytes.
Ardestani, Goli; Mehregan, Aujan; Fleig, Andrea; Horgen, F David; Carvacho, Ingrid; Fissore, Rafael A.
Afiliación
  • Ardestani G; Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, 661 North Pleasant Street, Amherst, MA, 01003, USA.
  • Mehregan A; Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, 661 North Pleasant Street, Amherst, MA, 01003, USA.
  • Fleig A; Center for Biomedical Research at The Queen's Medical Center and University of Hawaii Cancer Center and John A. Burns School of Medicine at the University of Hawaii, Honolulu, HI, 96813, USA.
  • Horgen FD; Department of Natural Sciences, Hawaii Pacific University, Kaneohe, HI, 96744, USA.
  • Carvacho I; Department of Biology and Chemistry, Faculty of Basic Sciences, Universidad Católica del Maule, 3480112, Talca, Chile.
  • Fissore RA; Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, 661 North Pleasant Street, Amherst, MA, 01003, USA. Electronic address: rfissore@vasci.umass.edu.
Cell Calcium ; 87: 102181, 2020 05.
Article en En | MEDLINE | ID: mdl-32097818
Prior to maturation, mouse oocytes are arrested at the germinal vesicle (GV) stage during which they experience constitutive calcium (Ca2+) influx and spontaneous Ca2+ oscillations. The oscillations cease during maturation but Ca2+ influx continues, as the oocytes' internal stores attain maximal content at the culmination of maturation, the metaphase II stage. The identity of the channel(s) that underlie this Ca2+ influx has not been completely determined. GV and matured oocytes are known to express three Ca2+ channels, CaV3.2, TRPV3 and TRPM7, but females null for each of these channels are fertile and their oocytes display minor modifications in Ca2+ homeostasis, suggesting a complex regulation of Ca2+ influx. To define the contribution of these channels at the GV stage, we used different divalent cations, pharmacological inhibitors and genetic models. We found that the three channels are active at this stage. CaV3.2 and TRPM7 channels contributed the majority of Ca2+ influx, as inhibitors and oocytes from homologous knockout (KO) lines showed severely reduced Ca2+ entry. Sr2+ influx was promoted by CaV3.2 channels, as Sr2+ oscillations were negligible in CaV3.2-KO oocytes but robust in control and Trpv3-KO GV oocytes. Mn2+ entry relied on expression of CaV3.2 and TRPM7 channels, but Ni2+ entry depended on the latter. CaV3.2 and TRPV3 channels combined to fill the Ca2+ stores, although CaV3.2 was the most impactful. Studies with pharmacological inhibitors effectively blocked the influx of divalent cations, but displayed off-target effects, and occasionally agonist-like properties. In conclusion, GV oocytes express channels mediating Ca2+ and other divalent cation influx that are pivotal for fertilization and early development. These channels may serve as targets for intervention to improve the success of assisted reproductive technologies.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oocitos / Cationes Bivalentes / Calcio / Homeostasis Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Cell Calcium Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oocitos / Cationes Bivalentes / Calcio / Homeostasis Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Cell Calcium Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos