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Galectin 15 (LGALS15) functions in trophectoderm migration and attachment
Author(s) -
Farmer Jennifer L.,
Burghardt Robert C.,
Jousan F. Dean,
Hansen Peter J.,
Bazer Fuller W.,
Spencer Thomas E.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.07-9308com
Subject(s) - blastocyst , trophoblast , staurosporine , microbiology and biotechnology , biology , cell migration , embryo , cleavage (geology) , chemistry , cell , embryogenesis , phosphorylation , protein kinase a , placenta , genetics , pregnancy , paleontology , fetus , fracture (geology)
Galectin 15 (LGALS15) is expressed specifically by the endometrial luminal epithelium (LE) of the ovine uterus in concert with blastocyst growth, elongation, and implantation. LGALS15 contains a predicted carbohydrate recognition domain (CRD) as well as LDV and RGD recognition sequences for integrin binding. Studies tested the hypothesis that LGALS15 is a secreted regulator of blastocyst development, as well as growth, migration, adhesion, and apoptosis of tro‐phoblast. Bovine embryos were produced in vitro by standard conditions, and putative zygotes were cultured in the presence of recombinant ovine LGALS15. Rates of embryo cleavage and blastocyst formation were not affected by LGALS15. LGALS15 moderately increased proliferation of ovine trophectoderm (oTr) cells. Staurosporine elicited apoptosis of oTr cells, which could be partially inhibited by LGALS15. Migration of oTr cells was stimulated by LGALS15 that was dependent on Jun N‐terminal kinase (JNK). A dose‐dependent increase in oTr cell attachment to LGALS15 was found that could be inhibited by cyclic GRGDS, but not GRADS, peptides. Mutation of the LDVRGD integrin binding sequence of LGALS15 to LADRAD decreased its ability to promote oTr cell attachment, whereas mutation of the CRD had little effect. LGALS15 induced formation of robust focal adhesions in oTr cells that was abolished by mutation of the LDVRGD sequence. Collectively, these results support the hypothesis that LGALS15 stimulates trophectoderm cell migration and attachment via integrin binding and activation which are critical to blastocyst elongation and implantation.—Farmer, J. L., Burghardt, R. C., Jousan, F. D., Hansen, P. J., Bazer, F. W., Spencer, T. E. Galectin 15 (LGALS15) functions in trophectoderm migration and attachment. FASEB J. 22, 548–560 (2008)