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과산화수소와 동결에 의해 유도된 생쥐와 소 수정란의 사멸에 있어서 칼륨 통로의 역할Role of K+ Channels in H2O2- and Cryo-induced Apoptosis of Mouse and Bovine Embryos

Other Titles
Role of K+ Channels in H2O2- and Cryo-induced Apoptosis of Mouse and Bovine Embryos
Authors
최창용김창운강다원한재희
Issue Date
2014
Publisher
사단법인 한국동물생명공학회
Keywords
apoptosis; antioxidant; cryopreservation; K+ channel
Citation
한국동물생명공학회지, v.29, no.3, pp 249 - 255
Pages
7
Indexed
KCI
Journal Title
한국동물생명공학회지
Volume
29
Number
3
Start Page
249
End Page
255
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/19698
ISSN
2671-4639
Abstract
Programmed cell death or apoptosis is associated with changes in K+ concentration in many cell types. Recentstudies have demonstrated that two-pore domain K+ (K2P) channels are involved in mouse embryonic development andapoptotic volume decrease of mammalian cells. In cerebellar granule neurons that normally undergo apoptosis duringthe early developmental stage, TASK-1 and TASK-3, members of K2P channels, were found to be critical for celldeath. This study was performed to identify the role of K+ channels in the H2O2-induced or cryo-induced cell deathof mouse and bovine embryos. Mouse and bovine two-cell stage embryos (2-cells) exposed to H2O2 for 4 h sufferedfrom apoptosis. The 2-cells showed positive TUNEL staining. Treatment with high concentration of KCl (25mM)inhibited H2O2-induced apoptosis of 2-cells by 19%. Cryo-induced death in bovine blastocysts showed positive TUNELstaining only in the cells near the plasma membrane. Cryoprotectant supplemented with 25 mM KCl reduced apoptosisslightly compared to cryoprotectant supplemented with 5 mM KCl. However, the combination of antioxidants (β-mercaptoethanol) with 25 mM KCl significantly decreased the rate of H2O2-induced and cryo-induced apoptosiscompared to treatments with only antioxidants or 25 mM KCl. These results show that blockage of K+ channel effluxfor a short-time reduces H2O2- and cryo-induced apoptosis in mouse and bovine embryos. Our findings suggest thatapoptosis in mouse and bovine embryos might be controlled by modulation of K+ channels which are highly expressedin a given cell type.
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