13 research outputs found
DNA repair mechanisms in mammalian germ cells
Mammalian germ cells encounter several
types of DNA damage. This damage is almost
completely repaired in a short period of time to provide
the maintenance of genomic integrity. The main repair
mechanisms operating in mammalian germline cells are:
nucleotide excision repair (NER), base excision repair
(BER), mismatch repair (MMR), DNA double strand
break repair (DSBR), and post replication repair (PRR).
Currently, there are relatively few publications that
summarize basic information and new findings on DNA
repair mechanisms used in mammalian germ cells. In the
present article, we review the studies that discuss repair
mechanisms operating in the female and male germ
cells. We then survey some of the recent discoveries
made in this field
Particular functions of estrogen and progesterone in establishment of uterine receptivity and embryo implantation
The process of embryo implantation requires
synchronized development of blastocyst and timely
establishment of uterine receptivity. Establishment of
uterine receptivity, preimplantation embryo development
and embryo implantation events are mainly regulated by
certain factors, including cytokines, chemokines, growth
factors and steroid hormones. Recent studies suggest that
steroid hormones, especially estrogen and progesterone,
play important roles in supporting endometrial
preparations to establish endometrial receptivity. Timely
establishment of endometrial receptivity is a crucial
process for providing successful embryo implantation.
Although many investigations until now have been
performed to precisely understand the effects of estrogen
and progesterone on acquiring uterine receptivity and
embryo implantation in humans and rodents, there are
limited numbers of studies that largely focus on this
subject. Therefore, in this article we discuss the studies
associated with significant functions of estrogen and
progesterone in establishing receptive endometrium and
the process of embryo implantation in humans and
rodents
Superovulation alters embryonic poly(A)-binding protein (Epab) and poly(A)-binding protein, cytoplasmic 1 (Pabpc1) gene expression in mouse oocytes and early embryos
WOS: 000368127000013PubMed ID: 25034140Embryonic poly(A)-binding protein (EPAB) and poly(A)-binding protein, cytoplasmic 1 (PABPC1) play critical roles in translational regulation of stored maternal mRNAs required for proper oocyte maturation and early embryo development in mammals. Superovulation is a commonly used technique to obtain a great number of oocytes in the same developmental stages in assisted reproductive technology (ART) and in clinical or experimental animal studies. Previous studies have convincingly indicated that superovulation alone can cause impaired oocyte maturation, delayed embryo development, decreased implantation rate and increased postimplantation loss. Although how superovulation results in these disturbances has not been clearly addressed yet, putative changes in genes related to oocyte and early embryo development seem to be potential risk factors. Thus, the aim of the present study was to determine the effect of superovulation on Epab and Pabpc1 gene expression. To this end, low- (5IU) and high-dose (10IU) pregnant mare's serum gonadotropin (PMSG) and human chorionic gonadotrophin (hCG) were administered to female mice to induce superovulation, with naturally cycling female mice serving as controls. Epab and Pabpc1 gene expression in germinal vesicle (GV) stage oocytes, MII oocytes and 1- and 2-cell embryos collected from each group were quantified using quantitative reverse transcription-polymerase chain reaction. Superovulation with low or high doses of gonadotropins significantly altered Epab and Pabpc1 mRNA levels in GV oocytes, MII oocytes and 1- and 2-cell embryos compared with their respective controls (P<0.05). These changes most likely lead to variations in expression of EPAB- and PABPC1-regulated genes, which may adversely influence the quality of oocytes and early embryos retrieved using superovulation.Akdeniz University [2008.01.0103.006]This study was supported by a grant from the Akdeniz University Research Fund (2008.01.0103.006). The authors thank Donald Desmond for helpful comments on and corrections to this article