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Clustered microRNAs: The molecular mechanism supporting the maintenance of luteal function during early pregnancy
Author(s) -
Przygrodzka Emilia,
Sokołowska Gabriela,
Myszczynski Kamil,
Krawczynski Kamil,
Kaczmarek Monika M.
Publication year - 2020
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.201903007rr
Subject(s) - corpus luteum , conceptus , luteal phase , microrna , biology , gene expression , function (biology) , endocrinology , andrology , medicine , gene , pregnancy , microbiology and biotechnology , ovary , hormone , fetus , genetics
MicroRNAs (miRNAs) are recognized as the important regulators of ovarian function. However, little is known about the hormonal regulation of miRNA expression and the role of the specific miRNA‐mRNA interactions in corpus luteum. Therefore, the present study was undertaken to determine: (a) the expression of miRNAs in the corpus luteum in early pregnancy vs regression; (b) the effect of conceptus and uterine signals in the expression of selected miRNAs; and (c) the role of specific miRNA‐mRNA interactions in the molecular changes and secretory function of the corpus luteum in the pig. The results showed that the majority of miRNAs differentially expressed in the corpus luteum in early pregnancy vs regression belong to independent clusters (eg, miR‐99b, miR‐532), which are highly conserved among different animal species. The main conceptus signal in the pig (17β‐estradiol) elevated the luteal expression of the miR‐99b cluster and lowered the expression of NR4A1 and AKR1C1 , the genes involved in corpus luteum regression. Furthermore, the delivery of miR‐99b cluster mimics to luteal tissue concomitantly decreased NR4A1 and AKR1C1 expression and enhanced progesterone secretion. The present study demonstrated that conceptus signals can support the maintenance of luteal function during pregnancy by clustered miRNA‐stimulated pathways, governing the expression of genes involved in luteal regression.