“…The JAK-STAT signaling pathway sustains and stimulates the growth of primordial follicles in women, thereby regulating the oocyte growth process and consequently female fertility [44,45]. Additionally, leptin inhibits uterine contractions in mice by stimulating the JAK-STAT signaling pathway [46]. The characterization of miRNA and mRNA expression profiles in hypothalamic tissues of high-and low-follicular fertility goats reveals that the identified differential expressed genes are significantly enriched in the JAK-STAT signaling pathway [47,48].…”
MicroRNA (miRNA) is a type of endogenous short−stranded ncRNA that influences many biological processes such as animal growth, development and metabolism. The thyroid gland is an important endocrine gland in sheep, and an increasing number of studies have shown that the thyroid gland plays an important role in animal reproduction, but the molecular mechanisms of the thyroid gland in sheep reproduction are poorly understood. In this study, RNA-seq was used to detect transcriptome expression patterns in the thyroid gland between the follicular phase (FP) and luteal phase (LP) in FecB BB (MM) and FecB ++ (ww) small-tail Han (STH) sheep, respectively, and to identify differentially expressed miRNAs (DEMs) associated with reproduction. Bioinformatic analysis of the target genes of these DEMs revealed that they can be enriched in multiple GO terms associated with the reproductive process in animals and in the KEGG signaling pathway. The miRNA–mRNA coexpression network revealed that oar-miR-133 and oar-miR-370-3p may play an important role in sheep reproduction. The results of the dual-luciferase reporter assay suggest a possible targeting relationship between novel-51 and TARBP2. These results provided a novel resource for elucidating regulatory mechanisms underlying STH sheep prolificacy.
“…The JAK-STAT signaling pathway sustains and stimulates the growth of primordial follicles in women, thereby regulating the oocyte growth process and consequently female fertility [44,45]. Additionally, leptin inhibits uterine contractions in mice by stimulating the JAK-STAT signaling pathway [46]. The characterization of miRNA and mRNA expression profiles in hypothalamic tissues of high-and low-follicular fertility goats reveals that the identified differential expressed genes are significantly enriched in the JAK-STAT signaling pathway [47,48].…”
MicroRNA (miRNA) is a type of endogenous short−stranded ncRNA that influences many biological processes such as animal growth, development and metabolism. The thyroid gland is an important endocrine gland in sheep, and an increasing number of studies have shown that the thyroid gland plays an important role in animal reproduction, but the molecular mechanisms of the thyroid gland in sheep reproduction are poorly understood. In this study, RNA-seq was used to detect transcriptome expression patterns in the thyroid gland between the follicular phase (FP) and luteal phase (LP) in FecB BB (MM) and FecB ++ (ww) small-tail Han (STH) sheep, respectively, and to identify differentially expressed miRNAs (DEMs) associated with reproduction. Bioinformatic analysis of the target genes of these DEMs revealed that they can be enriched in multiple GO terms associated with the reproductive process in animals and in the KEGG signaling pathway. The miRNA–mRNA coexpression network revealed that oar-miR-133 and oar-miR-370-3p may play an important role in sheep reproduction. The results of the dual-luciferase reporter assay suggest a possible targeting relationship between novel-51 and TARBP2. These results provided a novel resource for elucidating regulatory mechanisms underlying STH sheep prolificacy.
“…All of these findings suggest that modulation of the arachidonic acid metabolic pathway may be a prospective therapeutic strategy to alleviate symptoms in women with RSA. It has also been reported that the adipokine leptin can inhibit spontaneous and oxytocin-induced myometrial contractions by increasing NO and cGMP through stimulation of short-type leptin receptors and activation of the NO pathway in a JAK/STAT-dependent manner [ 87 ]. However, this trial demonstrated the inhibitory effect of leptin on uterine contractions only in late pregnancy, and it is not yet known whether it can be used in early pregnancy to reduce the incidence of spontaneous miscarriage.…”
Section: Abnormal Metabolism and Miscarriagementioning
Miscarriage is the most common complication of pregnancy. The most common causes of early miscarriage are chromosomal abnormalities of the embryo, maternal endocrine abnormalities, organ malformations, and abnormal immune factors. Late miscarriages are mostly caused by factors such as cervical insufficiency. However, the causes of 50% of miscarriages remain unknown. Recently, increasing attention has been given to the role of metabolic abnormalities in miscarriage. In this review, we mainly discuss the roles of four major metabolic pathways (glucose, lipid, and amino acid metabolism, and oxidation‒reduction balance) in miscarriage and the metabolism-related genes that lead to metabolic disorders in miscarriage. Depending on aetiology, the current treatments for miscarriage include hormonal and immunological drugs, as well as surgery, while there are few therapies for metabolism. Therefore, we also summarize the drugs for metabolism-related targets. The study of altered metabolism underlying miscarriage not only helps us to understand the mechanisms involved in miscarriage but also provides an important basis for clinical research on new therapies.
“…In addition, as described by Childs et al leptin-deficient mice are infertile, and the administration of exogenous LEP is able to restore fertility [7]. LEP exerts its actions through its receptor, LEPR, a single transmembrane protein made of 874 amino acids, expressed in the brain and peripheral tissues as kidneys, lungs, stomach, endometrium, placenta and umbilical cord [8,9]. Not only LEP alterations but also LEPR ones seem to have repercussions for reproduction and pregnancy; Pérez-Pérez et al theorized that LEP and LEPR anomalies could be implicated in the pathogenesis of recurrent miscarriage, pre-eclampsia and intrauterine growth restriction [4].…”
It has been proven that single-nucleotide polymorphisms (SNPs) in LEP and LEPR genes could predispose individuals to an increased risk of pregnancy adverse outcomes (PAOs) such as recurrent pregnancy loss (RPL) and pre-eclampsia. Preterm birth (PTB) is the leading cause of infant mortality. We decided to investigate the correlation between PTB and LEP and LEPR SNPs. The study cohort included families who underwent spontaneous PTB and control samples of families who had at-term-born (≥37 weeks of gestational age) children. Swabs were performed by rubbing the sticky end for about 30 s on the gum and on the inside of the cheek, allowing us to collect the flaking cells of the oral mucosa. Genotyping of the three SNPs—LEPRA668G, LEPG2548A and A19G—was carried out via an ARMS-MAMA real-time PCR procedure, as previously described. Regarding LEPG2548A, we found that the most expressed genotype in infants both in the preterm and the at-term group was AG; however, we did not discover any statistically significant difference (p = 0.97). Considering LEPA19G, none among the infants and parents were found to carry the AA genotype. No statistically significant differences were found between children, mothers and fathers belonging to preterm and at-term groups. We did not find a statistically significant association in newborns and their mother, but our results show a statistical correlation with the LEPRA668G genotype GG of the father. This fact can contribute to defining genetic risk factors for PTB. Further studies are certainly needed to better clarify the role of genetics in influencing preterm delivery.
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