A trial to overcome the injury caused by chilling/heat stress in oocytes/embryos by controlling temperature-sensitive channel activities

2016 Fiscal Year Final Research Report

• Project/Area Number: 26292170
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Integrative animal science
• Research Institution: Kochi University
• Principal Investigator: EDASHIGE Keisuke 高知大学, 教育研究部総合科学系, 教授 (30175228)
• Co-Investigator(Kenkyū-buntansha): 高橋 昌志 北海道大学, 農学研究院, 教授 (10343964) ; 越本 知大 宮崎大学, フロンティア科学実験総合センター, 教授 (70295210) ; 松川 和嗣 高知大学, 教育研究部総合科学系生命環境医学部門, 准教授 (00532160) ; 葛西 孫三郎 高知大学, 教育研究部総合科学系, 教授 (60152617)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 低温傷害 / TRPチャンネル / ブタ卵子 / ブタ胚 / ウシ胚 / 高温傷害

Outline of Final Research Achievements

In this study, we examined whether a low-temperature sensitive transient receptor potential (TRP) channel was involved in the chilling injury of pig oocytes/embryos. The mRNA of TRPA1, which is sensitive to the temperature at lower than 17oC, was expressed in pig oocytes and embryos at various stages. Exposure of oocytes/embryos to 15oC for 15 min markedly decreased their viability. Exposure of oocytes to 15oC increased intracellular Ca2+ immediately. The pretreatment of oocytes with AP-18, a specific inhibitor for TRPA1, suppressed the increase in their intracellular Ca2+ and the decrease in their viability by the exposure to 15oC. These results indicate that TRPA1 is involved in the chilling injury of pig oocytes/embryos, and that the injury can be circumvented by suppressing TRPA1 activity. Our findings would be useful for developing a cryopreservation method for pig oocytes/embryos.

Free Research Field

家畜繁殖学