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The corpus luteum is an endocrine gland that synthesizes the steroid hormone progesterone. luteinizing hormone (LH) is a key luteotropic hormone that stimulates ovulation, luteal development, progesterone biosynthesis, and maintenance of the corpus luteum. Luteotropic and luteolytic factors precisely regulate luteal structure and function; yet, despite recent scientific progress within the past few years, the exact mechanisms remain largely unknown. In the present review, we summarize the recent progress towards understanding cellular changes induced by LH in steroidogenic luteal cells. Herein, we will focus on the effects of LH on inter-organelle communication and steroid biosynthesis, and how LH regulates key protein kinases (i.e., AMPK and MTOR) responsible for controlling steroidogenesis and autophagy in luteal cells.

Conceptus-derived interferon-tau (IFNT) initiates maternal recognition of pregnancy in ewes by paracrine actions on the endometrium and endocrine action on the corpus luteum (CL). To examine the effect of IFNT on the CL without inducing IFN-stimulated genes (ISGs) in the endometrium, recombinant ovine IFNT (roIFNT) or bovine serum albumin was delivered directly into CLs via osmotic pumps at a rate of 10, 50, or 100 ng/h from days 9 to 12 of the estrous cycle. Endometrial and CL samples were collected on day 12. 50 ng/h of roIFNT induced ISG15 in the CL on day 12 without affecting endometrial ISG15 concentrations. In a second experiment, roIFNT (50 ng/h) was infused into the CL from days 10 to 17 of the estrous cycle and serum samples were collected daily. Serum progesterone concentrations were significantly higher from days 15 to 17 in roIFNT-infused ewes compared to controls. Levels of LHCGR, STAR, CYP11A1, HSL, OPA1, and protein kinase A mRNA and proteins were higher in the roIFNT-infused CLs compared to the controls. Levels of ISG15 and MX1 mRNA increased in the CLs of roIFNT-infused ewes but not in the endometrium. Endometrial ESR1 mRNA and protein concentrations were higher in the controls compared to roIFNT-infused ewes. In conclusion, intra-luteal delivery of roIFNT induced ISGs, stabilized steroidogenesis in the CL, and delayed luteolysis without inducing endometrial IFN-stimulated genes. Inhibition of ESR1 in the endometrium of roIFNT-infused ewes was observed suggesting that direct delivery of IFNT to the CL has an additional anti-luteolytic effect on the endometrium. Summary Sentence Interferon-tau induces interferon-stimulated genes, delays luteolysis, and stabilizes steroidogenesis in the ovine corpus luteum. Graphical Abstract

The microRNA (miRNA) processing enzyme Dicer1 is required for zygotic and embryonic development, but the early embryonic lethality of Dicer1 null alleles in mice has limited our ability to address the role of Dicer1 in normal mouse growth and development. To address this question, we used a mouse mutant with a hypomorphic Dicer1 allele (Dicer(d/d)) and found that Dicer1 deficiency resulted in female infertility. This defect in female Dicer(d/d) mice was caused by corpus luteum (CL) insufficiency and resulted, at least in part, from the impaired growth of new capillary vessels in the ovary. We found that the impaired CL angiogenesis in Dicer(d/d) mice was associated with a lack of miR17-5p and let7b, 2 miRNAs that participate in angiogenesis by regulating the expression of the antiangiogenic factor tissue inhibitor of metalloproteinase 1. Furthermore, injection of miR17-5p and let7b into the ovaries of Dicer(d/d) mice partially normalized tissue inhibitor of metalloproteinase 1 expression and CL angiogenesis. Our data indicate that the development and function of the ovarian CL is a physiological process that appears to be regulated by miRNAs and requires Dicer1 function.

Cyclic regression of the ovarian corpus luteum, the endocrine gland responsible for progesterone production, involves rapid matrix remodeling. Despite fibroblasts in other systems being known for producing and maintaining extracellular matrix, little is known about fibroblasts in the functional or regressing corpus luteum. Vast transcriptomic changes occur in the regressing corpus luteum, among which are reduced levels of vascular endothelial growth factor A (VEGFA) and increased expression of fibroblast growth factor 2 (FGF2) after 4 and 12 h of induced regression, when progesterone is declining and the microvasculature is destabilizing. We hypothesized that FGF2 activates luteal fibroblasts. Analysis of transcriptomic changes during induced luteal regression revealed elevations in markers of fibroblast activation and fibrosis, including fibroblast activation protein (FAP), serpin family E member 1 (SERPINE1), and secreted phosphoprotein 1 (SPP1). To test our hypothesis, we treated bovine luteal fibroblasts with FGF2 to measure downstream signaling, type 1 collagen production, and proliferation. We observed rapid and robust phosphorylation of various signaling pathways involved in proliferation, such as ERK, AKT, and STAT1. From our longer-term treatments, we determined that FGF2 has a concentration-dependent collagen-inducing effect, and that FGF2 acts as a mitogen for luteal fibroblasts. FGF2-induced proliferation was greatly blunted by inhibition of AKT or STAT1 signaling. Our results suggest that luteal fibroblasts are responsive to factors that are released by the regressing bovine corpus luteum, an insight into the contribution of fibroblasts to the microenvironment in the regressing corpus luteum. Summary Sentence Elevation of FGF2 expression during luteal regression may lead to alterations in the luteal microenvironment by stimulating proliferation of luteal fibroblasts and production of extracellular matrix. Graphical Abstract

Previously, we demonstrated the expression of visfatin in porcine reproductive tissues and its effect on pituitary endocrinology. The objective of this study was to examine the visfatin effect on the secretion of steroid (P 4 , E 2 ) and prostaglandin (PGE 2 , PGF 2α ), the mRNA and protein abundance of steroidogenic markers (STAR, CYP11A1, HSD3B, CYP19A1), prostaglandin receptors (PTGER2, PTGFR), insulin receptor (INSR), and activity of kinases (MAPK/ERK1/2, AKT, AMPK) in the porcine corpus luteum. We noted that the visfatin effect strongly depends on the phase of the estrous cycle: on days 2–3 and 14–16 it reduced P 4 , while on days 10–12 it stimulated P 4 . Visfatin increased secretion of E 2 on days 2–3, PGE 2 on days 2–3 and 10–12, reduced PGF 2α release on days 14–16, as well as stimulated the expression of steroidogenic markers on days 10–12 of the estrous cycle. Moreover, visfatin elevated PTGER mRNA expression and decreased its protein level, while we noted the opposite changes for PTGFR. Additionally, visfatin activated ERK1/2, AKT, and AMPK, while reduced INSR phosphorylation. Interestingly, after inhibition of INSR and signalling pathways visfatin action was abolished. These findings suggest a regulatory role of visfatin in the porcine corpus luteum.

In cattle, conceptus development after elongation relies on well-characterized, paracrine interactions with the hosting maternal reproductive tract. However, it was unrecognized previously that the pre-hatching, pre-implantation bovine embryo also engages in biochemical signalling with the maternal uterus. Our recent work showed that the embryo modified the endometrial transcriptome in vivo . Here, we hypothesized that the embryo modulates the biochemical composition of the uterine luminal fluid (ULF) in the most cranial portion of the uterine horn ipsilateral to the corpus luteum. Endometrial samples and ULF were collected post-mortem from sham-inseminated cows and from cows inseminated and detected pregnant 7 days after oestrus. We used quantitative mass spectrometry to demonstrate that the pre-hatching embryo changes ULF composition in vivo . Embryo-induced modulation included an increase in concentrations of lipoxygenase-derived metabolites [12(S)-HETE, 15(S)-HETE] and a decrease in the concentrations of amino acids (glycine), biogenic amines (sarcosine), acylcarnitines and phospholipids. The changed composition of the ULF could be due to secretion or depletion of specific molecules, executed by either the embryo or the endometrium, but initiated by signals coming from the embryo. This study provides the basis for further understanding embryo-initiated modulation of the uterine milieu. Early embryonic signalling may be necessary to guarantee optimal development and successful establishment of pregnancy in cattle.

MicroRNAs (miRNAs) constitute a large family of noncoding RNAs, approximately 22 nucleotides long, which function as guide molecules in RNA silencing. Targeting most protein-coding transcripts, miRNAs are involved in nearly all developmental and pathophysiological processes in animals. To date, the regulatory roles of miRNAs in reproduction, such as fertilization, embryo development, implantation, and placenta formation, among others, have been demonstrated in numerous mammalian species, including domestic livestock such as pigs. Over the past years, it appeared that understanding the functions of miRNAs in mammalian reproduction can substantially improve our understanding of the biological challenges of successful reproductive performance. This review describes the current knowledge on miRNAs, specifically in relation to the peri-implantation period when the majority of embryonic mortality occurs in pigs. To present a broader picture of crucial peri-implantation events, we focus on the role of miRNA-processing machinery and miRNA–mRNA infarctions during the maternal recognition of pregnancy, leading to maintenance of the corpus luteum function and further embryo implantation. Furthermore, we summarize the current knowledge on cell-to-cell communication involving extracellular vesicles at the embryo–maternal interface in pigs. Finally, we discuss the potential of circulating miRNAs to serve as indicators of ongoing embryo–maternal crosstalk.

In the domestic cat ( Felis catus ), the corpus luteum (CL) is the main source of progestogen during pregnancy. Here, we studied gene expression changes in different life cycle stages of the CL of pseudopregnant cats to identify potential regulatory factors. Results revealed no support for different regression substages, which were previously defined on the basis of morphological examination analysis and intraluteal hormone content, as only a very low number of differentially expressed genes and no subclusters in PCA plot were detected. By comparing the regression stage with the developmental/maintenance stage, we detected a total of 6174 differentially expressed genes in the sample set, of which 2882 were upregulated and 3292 were downregulated. The large changes in the expression levels of some genes indicate that the endocrine function of the CL may not be restricted to progesterone (P4) secretion. The findings suggest that domestic cat CLs could also be a source of adipokines such as adiponectin or APELA. The expression of these genes is highly variable and reversed between stages. The life cycle and activity of CLs seem to be regulated by different factors, as genes encoding for the hormone receptors LHCGR and PAQR5 were more highly expressed in the development/maintenance stage, in contrast to this encoding for LEPR, which is higher expressed in regression stage. For regression stage, we identified different potential ways to modulate the cholesterol level and/or P4 concentration. Furthermore, we found differences from previous studies in other species for many genes that were studied in more detail, as well as when analysing functions and pathways. Our findings support the hypothesis that different stages of the CL life cycle in domestic cats can be characterized by changes in gene regulation and that CL life cycles are partly differentially regulated between species.

Despite the negative environmental and biologic effects, organophosphates have currently been widely used. We aimed to examine the possible negative effects of diazinon, a type of organophosphate, on rat ovarian tissue. Wistar Albino rats were divided into four groups. No treatment was given to control, olive oil was applied to sham group. Experimental groups were injected intraperitoneally with 30 and 60 mg/kg/day diazinon, respectively. 24 h later, ovarian tissues were extracted, preparated, examined via light and electron microscope. In the experimental groups granulosa and corpus luteum showed degenerative changes. Dilatation of endoplasmic reticulum cisterns and morphological alterations of mitochondria in granulosa cells were detected utrastructurally. Also, accumulation of lipid droplets and autophagic vacuoles was observed in cells of corpus luteum. A statistically significant dose-dependent decrease in superoxide dismutase and catalase reactivity and a statistically significant increase in caspase-3 expression in cells of atretic follicles and corpus luteum were observed. Results show that exposure to a single dose of diazinon may disrupt antioxidant system, trigger atresia in follicles and negatively effect corpus luteum functions. It was concluded that studies applying possible antioxidant treatments should be carried out to reduce and prevent the negative effects of diazinon on the reproductive system.

Formation and limited lifespan of corpus luteum (CL) are important for proper ovarian periodicity and fertility. Failed vascularization, imbalance between proliferation and apoptosis leads to luteal phase deficiency and infertility. The aim of this study was to examine the effect of vaspin on angiogenesis, apoptosis and proliferation as well as the involvement of 78-kDa glucose-regulated protein receptor (GRP78) and mitogen-activated kinase (MAP3/1) in these processes. Porcine luteal cells were incubated with vaspin (0.1-10 ng/mL) for 24 h to 72 h and then mRNA and protein expression of angiogenesis: vascular endothelial growth factor (VEGFA), fibroblast growth factor 2 (FGF2), angiopoietin 1 (ANGPT1), VEGFA receptors (VEGFR1, VEGFR2), apoptosis: caspase 3, bcl-2-like protein 4 (BAX), B-cell lymphoma (BCL2), and proliferation: proliferating cells nuclear antigen (PCNA), cyclin A factors as well as secretion of VEGFA, FGF2, ANGT1 were measured by real-time polymerase chain reaction (PCR), immunoblotting and enzyme-linked immunosorbent assay (ELISA), respectively. Moreover, apoptosis was assessed by caspase activity using the Caspase-Glo 3/7 assay, while proliferation was by alamarBlue. We found that vaspin enhanced luteal cell angiogenesis, proliferation, and significantly decreased apoptosis. Additionally, using GRP78 siRNA and the pharmacological inhibitor of MAP3/1 (PD98059), we observed that the effect of vaspin was reversed to the control level in all investigated processes. Taken together, our results suggest that vaspin is a new regulator of female fertility by direct regulation of CL formation and maintenance of luteal cell function.