Knowledge Sharing
2011.09.13
Compensatory role of EGF on embryonic development in LIF-deficient murine pre-implantation embryos
Annual Meeting of Taiwanese Society for Reproductive Medicine,Conference Paper Award
Compensatory role of EGF on embryonic development in LIF-deficient murine pre-implantation embryos
ZHENG EN-HUI 12, LIU ZHE YU 3, HUANG JUN-JIA 1, Zhong- Yi Chen 1, HUANG LI-XIANG 1, Maw-Sheng Lee 145
Lee Women’s Hospital 1, Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University 2, Cancer Center, China Medical University Hospital 3, Institute of Medicine, Chung Shan Medical University 4, Department of Obstetrics and Gynecology, China Medical University Hospital 5
Compensatory role of EGF on embryonic development in LIF-deficient murine pre-implantation embryos
ZHENG EN-HUI 12, LIU ZHE YU 3, HUANG JUN-JIA 1, Zhong- Yi Chen 1, HUANG LI-XIANG 1, Maw-Sheng Lee 145
Lee Women’s Hospital 1, Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University 2, Cancer Center, China Medical University Hospital 3, Institute of Medicine, Chung Shan Medical University 4, Department of Obstetrics and Gynecology, China Medical University Hospital 5
Leukemia inhibitory factor (LIF) is an essential factor for implantation and establishment of pregnancy. However, its role in the development of pre-implantation embryo remains controversy. Our previous studies in the inhibition of murine fertilized egg via LIF antisense oligonucleotide revealed LIF deficiency led to lower percentages of embryos developed from morula to blastocyst stage. Here we microinjected LIF antisense oligonucleotides into murine pronuclear stage embryo, and magnetic sorting was carried out for mRNA purification from embryos developed to morula.
After reverse transcription, a gene chip containing 9652 genes were applied for the gene expression analysis between control and treatment groups. Expression of 219 genes was down-regulated whereas that of 154 genes was elevated. Next we supplement LIF after microinjection of LIF antisense oligonucleotide, and we found up- and down-regulation of EGF expression by LIF deficiency and after LIF supplementation, respectively. In summary, our results suggest that EGF is able to compensate for LIF to maintain normal embryonic development in LIF-deficient embryos. However, the mechanism of compensation is unclear and awaits further investigation.
