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Caspase-3 gene expression in human luteinized granulosa cells is inversely correlated with the number of oocytes retrieved after controlled ovarian stimulation.

Authors :
Lobach VN
Casalechi M
Dela Cruz C
Pereira MT
Del Puerto HL
Reis FM
Source :
Human fertility (Cambridge, England) [Hum Fertil (Camb)] 2019 Apr; Vol. 22 (1), pp. 33-38. Date of Electronic Publication: 2017 Jul 25.
Publication Year :
2019

Abstract

Granulosa cells control oocyte maturation through paracrine signalling and changes to the microenvironment around the oocyte. Apoptosis occurs as a physiological mechanism of granulosa cell renewal, but how it relates with the ovarian response to induced ovulation is still unclear. Therefore, this study evaluated apoptosis-related gene expression levels in granulosa cells of patients undergoing controlled ovarian stimulation. We enrolled prospectively 59 consecutive IVF patients referred to a tertiary academic hospital for couple infertility treatment. Luteinized granulosa cells were isolated from follicular fluid and the RNA was extracted, reverse-transcribed and the gene expression of apoptosis inducers (caspase-3, caspase-8 and bax) and inhibitor (Bcl-2) was quantified by real-time polymerase chain reaction. Caspase-3 gene expression correlated negatively with the number of pre-ovulatory follicles (Spearman's r =  -0.308), the number of collected oocytes (r =  -0.451), the number of mature oocytes (r =  -0.526), the number of fertilized oocytes (r =  -0.439) and the number of viable embryos (r =  -0.443, all statistically significant at p < 0.02 level). No such associations were found with caspase-8, bax or bcl-2. These preliminary findings suggest that increased caspase-3 gene expression in granulosa cells is associated with a worse ovulatory response in humans.

Details

Language :
English
ISSN :
1742-8149
Volume :
22
Issue :
1
Database :
MEDLINE
Journal :
Human fertility (Cambridge, England)
Publication Type :
Academic Journal
Accession number :
28738699
Full Text :
https://doi.org/10.1080/14647273.2017.1356474