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Insulin‐like growth factor‐I promotes resistance of bovine preimplantation embryos to heat shock through actions independent of its anti‐apoptotic actions requiring PI3K signaling
Author(s) -
Jousan F. Dean,
Hansen Peter J.
Publication year - 2007
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20527
Subject(s) - biology , blastocyst , apoptosis , microbiology and biotechnology , heat shock protein , growth factor , pi3k/akt/mtor pathway , embryo , insulin like growth factor , signal transduction , programmed cell death , embryogenesis , receptor , genetics , gene
For the bovine preimplantation embryo, insulin‐like growth factor‐I (IGF‐I) is a survival factor that blocks the induction of apoptosis and reduces the decrease in development caused by heat shock. The first objective was to determine the signaling pathways whereby IGF‐I acts to increase embryo cell number while inhibiting heat‐shock induced apoptosis. Exposure of embryos to heat shock reduced cell number and increased percent apoptosis, but IGF‐I increased cell number and blocked induction of apoptosis caused by heat shock. Actions of IGF‐I to increase cell number were blocked by treatment with the mitogen activated protein kinase kinase (MAPKK) inhibitor PD 98059 whereas the phosphatidylinositol 3‐kinase (PI3K) inhibitor LY 294002 had no effect. Conversely, LY 294002 but not PD 98059 blocked actions of IGF‐I to inhibit induction of apoptosis caused by heat shock. The second objective was to determine whether IGF‐I blocks effects of heat shock on development to the blastocyst stage by preventing apoptosis. Culture of embryos with IGF‐I was effective in blocking the reduction in blastocyst development caused by heat shock—this action occurred even in the presence of LY 294002. Addition of another inhibitor of apoptosis, the caspase‐3 inhibitor z‐DEVD‐fmk, did not mimic the protective effects of IGF‐I on blastocyst development. Surprisingly, IGF‐I was not effective in blocking the reduction in blastocyst development caused by heat shock when cultured with z‐DEVD‐fmk. In conclusion, the anti‐apoptotic actions of IGF‐I require PI3K signaling while actions to promote proliferation require MAPKK signaling. Moreover, actions of IGF‐I to allow heat‐shocked embryos to continue development to the blastocyst stage are independent of its anti‐apoptotic effects. Mol. Reprod. Dev. © 2006 Wiley‐Liss, Inc.