BOR - Papers in Press, published online ahead of print
July 14, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.032102
BIOLOGY OF REPRODUCTION 71, 16651670 (2004)
DOI: 10.1095/biolreprod.104.032102
© 2004 by the Society for the Study of Reproduction, Inc.
Insulin-like Growth Factor-I as a Survival Factor for the Bovine Preimplantation Embryo Exposed to Heat Shock1
F.D. Jousan, and
P.J. Hansen2
Department of Animal Sciences, University of Florida, Gainesville, Florida 32611-0910
Insulin-like growth factor-I (IGF-I) is a survival factor for preimplantation mammalian embryos exposed to stress. One stress that compromises preimplantation embryonic development is elevated temperature (i.e., heat shock). Using bovine embryos produced in vitro as a model, it was hypothesized that IGF-I would protect preimplantation embryos by reducing the effects of heat shock on total cell number, the proportion of blastomeres that undergo apoptosis, and the percentage of embryos developing to the blastocyst stage. In experiment 1, embryos were cultured with or without IGF-I; on Day 5 after insemination, embryos
16 cells were cultured at 38.5°C for 24 h or were subjected to 41°C for 9 h followed by 38.5°C for 15 h. Heat shock reduced the total cell number at 24 h after initiation of heat shock and increased the percentage of blastomeres that were apoptotic. Effects of heat shock were less for IGF-I-treated embryos. Experiment 2 was conducted similarly except that embryos were allowed to develop to Day 8 after insemination. The percentage reduction in blastocyst development for heat-shocked embryos compared with those maintained at 38.5°C was less for embryos cultured with IGF-I than for control embryos. Heat shock reduced the total cell number in blastocysts and increased the percentage of blastomeres that were apoptotic, whereas IGF-I-treated embryos had increased total cell number and a reduced percentage of apoptosis. Taken together, these results demonstrate that IGF-I can serve as a survival factor for preimplantation bovine embryos exposed to heat shock by reducing the effects of heat shock on development and apoptosis.
1 This research was supported in part by the following grants from the U.S. Department of Agriculture: IFAFS 2001-52101-11318, TSTAR 2001-34135-11150, and NRICGP 2002-35203-12664. This is Journal Series No. R-10240 of the Florida Agricultural Experiment Station.
2 Correspondence: Peter J. Hansen, Department of Animal Sciences, University of Florida, P.O. Box 110910, Gainesville, FL 32611-0910. FAX: 352 392 5595; hansen{at}animal.ufl.edu
Copyright © 2004 by the Society for the Study of Reproduction.