Endoplasmic reticulum stress in periimplantation embryos.
- Author:
Marek MICHALAK
1
;
Myung Chan GYE
Author Information
- Publication Type:In Vitro ; Review
- Keywords: Embryos; Endoplasmic reticulum stress; Oocytes; Unfolded protein response coping response
- MeSH: Blastocyst; Cell Death; Cell Survival; Diagnosis; Embryonic Development; Embryonic Structures*; Endoplasmic Reticulum; Endoplasmic Reticulum Stress*; Female; Homeostasis; Oocytes; Organogenesis; Placentation; Pregnancy; Unfolded Protein Response
- From:Clinical and Experimental Reproductive Medicine 2015;42(1):1-7
- CountryRepublic of Korea
- Language:English
- Abstract: Stress coping mechanisms are critical to minimize or overcome damage caused by ever changing environmental conditions. They are designed to promote cell survival. The unfolded protein response (UPR) pathway is mobilized in response to the accumulation of unfolded proteins, ultimately in order to regain endoplasmic reticulum (ER) homeostasis. Various elements of coping responses to ER stress including Perk, Ask1, Bip, Chop, Gadd34, Ire1, Atf4, Atf6, and Xbp1 have been identified and were found to be inducible in oocytes and preimplantation embryos, suggesting that, as a normal part of the cellular adaptive mechanism, these coping responses, including the UPR, play a pivotal role in the development of preimplantation embryos. As such, the UPR-associated molecules and pathways may become useful markers for the potential diagnosis of stress conditions for preimplantation embryos. After implantation, ER stress-induced coping responses become physiologically important for a normal decidual response, placentation, and early organogenesis. Attenuation of ER stress coping responses by tauroursodeoxycholate and salubrinal was effective for prevention of cell death of cultured embryos. Further elucidation of new and relevant ER stress coping responses in periimplantation embryos might contribute to a comprehensive understanding of the regulation of normal development of embryonic development and potentiation of embryonic development in vitro.
