K+ efflux through two-pore domain K+ channels is required for mouse embryonic developmentopen access
- Authors
- Hur, Chang-Gi; Kim, Eun-Jin; Cho, Seong-Keun; Cho, Young-Woo; Yoon, Sook-Young; Tak, Hyun-Min; Kim, Chang-Woon; Choe, Changyong; Han, Jaehee; Kang, Dawon
- Issue Date
- May-2012
- Publisher
- BIOSCIENTIFICA LTD
- Citation
- REPRODUCTION, v.143, no.5, pp.625 - 636
- Indexed
- SCIE
SCOPUS
- Journal Title
- REPRODUCTION
- Volume
- 143
- Number
- 5
- Start Page
- 625
- End Page
- 636
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/22185
- DOI
- 10.1530/REP-11-0225
- ISSN
- 1470-1626
- Abstract
- Numerous studies have suggested that K+ channels regulate a wide range of physiological processes in mammalian cells. However, little is known about the specific function of K+ channels in germ cells. In this study, mouse zygotes were cultured in a medium containing K+ channel blockers to identify the functional role of K+ channels in mouse embryonic development. Voltage-dependent K+ channel blockers, such as tetraethylammonium and BaCl2, had no effect on embryonic development to the blastocyst stage, whereas K-2P channel blockers, such as quinine, selective serotonin reuptake inhibitors (fluoxetine, paroxetine, and citalopram), gadolinium trichloride, anandamide, ruthenium red, and zinc chloride, significantly decreased blastocyst formation (P<0.05). RT-PCR data showed that members of the K-2P channel family, specifically KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9, were expressed in mouse oocytes and embryos. In addition, their mRNA expression levels, except Kcnk3, were up-regulated by above ninefold in morula-stage embryos compared with 2-cell stage embryos (2-cells). Immunocytochemical data showed that KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9 channel proteins were expressed in the membrane of oocytes, 2-cells, and blastocysts. Each siRNA injection targeted at Kcnk2, Kcnk10, Kcnk4, Kcnk3, and Kcnk9 significantly decreased blastocyst formation by similar to 38% compared with scrambled siRNA injection (P<0.05). The blockade of K-2P channels acidified the intracellular pH and depolarized the membrane potential. These results suggest that K-2P channels could improve mouse embryonic development through the modulation of gating by activators. Reproduction (2012) 143 625-636
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