Calcium signaling in human preimplantation development: A review

Authors
Citation
J. Tesarik, Calcium signaling in human preimplantation development: A review, J AS REPROD, 16(4), 1999, pp. 216-220
Citations number
30
Categorie Soggetti
Reproductive Medicine
Journal title
JOURNAL OF ASSISTED REPRODUCTION AND GENETICS
ISSN journal
10580468 → ACNP
Volume
16
Issue
4
Year of publication
1999
Pages
216 - 220
Database
ISI
SICI code
1058-0468(199904)16:4<216:CSIHPD>2.0.ZU;2-9
Abstract
Purpose: Cell cycle-related calcium signals, bearing some similarity to tho se previously described in other animal species, have also been observed in human preimplantation embryos. These signals follow those occurring in bot h gametes during the period preceding fertilization and those induced by th e fertilizing spermatozoon in the oocyte after gamete fusion. Even though t he signals occurring during each of these distinct developmental periods ha ve different temporal and spatial characteristics, there may be a relations hip between them; in fact, abnormalities of calcium signals occurring in an earlier developmental period may be at the origin of abnormal signals duri ng later developmental periods. Methods: Possible mechanisms by which inadequate or truncated calcium signa ls call impair embryo development are discussed. Results: These mechanisms include complete failure of the second meiotic di vision, leading to triploidy; incomplete failure of the second meiotic divi sion, leading to de novo chromosomal numerical abnormalities; abnormal pron uclear development and function; abnormalities of the blastomere cell cycle , possibly leading to embryo cleavage arrest; and problems with blastomere allocation to embryonic cell lineages, leading to disproportionate developm ent of the inner cell mass and trophectoderm derivatives, which can be the origin of implantation failure or miscarriage. Conclusions: Future research should make it possible to decipher the nature of normal developmental signals, to determine the key checkpoints at which these signals are required to prevent the switch to apoptosis, and to exam ine the possibilities of therapeutic action at these checkpoints to rescue the endangered embryo for normal development.