Premium
Epidermal growth factor receptor and ligands in elongating bovine blastocysts
Author(s) -
Kliem Anne,
Tetens Frank,
Klonisch Thomas,
Grealy Maura,
Fischer Bernd
Publication year - 1998
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/(sici)1098-2795(199812)51:4<402::aid-mrd7>3.0.co;2-9
Subject(s) - biology , microbiology and biotechnology , epidermal growth factor receptor , epidermal growth factor , receptor , blastocyst , embryo , genetics , embryogenesis
Preimplantation development depends on multiple interactions between mother and embryo. The Epidermal Growth Factor Receptor (EGF‐R) and its ligands are potential components of the embryo‐maternal cross‐talk. Employing RT‐PCR, in situ hybridization, and immunohistochemistry, we investigated on mRNA and protein level the expression of EGF‐R, Epidermal Growth Factor (EGF), Transforming Growth Factor alpha (TGF‐α), and Heparin‐binding EGF‐like Growth Factor (HB‐EGF) in spherical and elongating bovine blastocysts between day 13 and day 16 of gestation, and in endometrium at day 13 of gestation. EGF‐R mRNA and protein were detected in trophoblast and endoderm cells of all blastocyst stages that were studied, and in luminal and some glandular epithelial cells of the endometrium at day 13. EGF protein was detected in both blastocysts and endometrial epithelium. TGF‐α transcripts and protein were present in blastocysts prior to and after elongation and in uterine glandular and luminal epithelium at day 13 of gestation. HB‐EGF mRNA and protein was shown in the endoderm, and the protein also was detected immunohistochemically in about 45% of the blastocysts. This presence of the EGF receptor‐ligand system in the endometrium and the preimplantation embryo at the time of blastocyst elongation suggests an important role for these growth factors during bovine preimplantation development. Mol. Reprod. Dev. 51:402–412, 1998. © 1998 Wiley‐Liss, Inc.