ICSI causes abnormal H3K9 methylation in the male pronuclei and growth retardation of mouse embryos.
- Author:
Na TANG
1
;
Xiao-Hong WANG
;
Xin-Xin LIANG
;
Jian-Bo LI
;
Dong WANG
;
Yuan LIU
;
Bo LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Embryonic Development; Female; Histones; metabolism; Jumonji Domain-Containing Histone Demethylases; metabolism; Male; Methylation; Mice; Mice, Inbred ICR; Pregnancy; Sperm Injections, Intracytoplasmic; adverse effects
- From: National Journal of Andrology 2013;19(7):593-598
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the safety of intracytoplasmic sperm injection (ICSI) in the mouse model.
METHODSWe simulated clinical ICSI technology and comprehensively evaluated it by parthenogenetic activation, immunofluorescence, embryo transplantation, examination of early implantation, and measurement of the crown-rump length (CRL).
RESULTSICSI significantly reduced the ability of preimplantation embryo development of the mouse, especially after the 8-cell stage (P < 0.01). The fluorescence of H3K9 dimethylation was abnormal at the male pronuclei of the embryos derived from ICSI. Further examination of the development of the transferred ICSI embryos indicated no significant difference in the rate of early implantation at E5. 5 days as compared with normal fertilization (P = 0.6), but the percentage of "normal embryos" was decreased significantly at E9.5 days (P < 0.01). Obvious growth retardation phenotype was observed even in the normal ICSI embryos at E9.5 days.
CONCLUSIONICSI might result in growth retardation of embryos by affecting H3K9 dimethylation in the male pronuclei.
