Maternal Tissues Research Articles

Molar pregnancy unveiled by DNA profiling: a rare forensic case study

BackgroundForensic DNA analysis is one of the most advanced tools in the criminal investigation. It is used successfully in solving offenses involving rape, paternity disputes, murder or attempt to murder, and dacoity as well as identification of mutilated body remains. DNA profiling is used to determine paternity in sexual offense cases where abortion takes place and the product of conception can be anywhere from 6 to 10 weeks of gestation to 8 months. In the present case, a tissue sample stated as a vesicular mole and blood samples of the mother and suspected father were submitted to the DNA division of our laboratory for paternity analysis.ResultsGenotyping results revealed a single allele at all the tested short tandem repeat (STR) loci. The allele obtained at each locus was common with the suspected father. Such type of genotype was very rare and not observed earlier; therefore, repeated analysis was done and the same genotype was obtained every time. DNA profiling revealed all the alleles in the vesicular mole to be of paternal origin only, devoid of any maternal alleles. After referring to books on gynecology, it was confirmed that the genotype obtained was of hydatidiform mole.ConclusionsIn this POCSO Act case, the product of conception (about 1.5 months old) was termed a vesicular mole, and blood samples of the mother and suspected father were sent for the DNA paternity test. STR profiling of the product of conception sample displayed no maternal tissue contamination and non-inheritance of maternal alleles, showing the case to be of molar pregnancy also called hydatidiform mole, a very rare phenomenon in the forensic scenario. After thorough analysis, the case was reported and it was the first of its kind to be reported in a forensic laboratory in Maharashtra, India.

Preeclampsia Is Associated With Complement Activation in Maternal and Fetal Circulation and Placental Tissue

Preeclampsia Is Associated With Complement Activation in Maternal and Fetal Circulation and Placental Tissue

Developing Genetic Engineering Techniques for Control of Seed Size and Yield.

Many signaling pathways regulate seed size through the development of endosperm and maternal tissues, which ultimately results in a range of variations in seed size or weight. Seed size can be determined through the development of zygotic tissues (endosperm and embryo) and maternal ovules. In addition, in some species such as rice, seed size is largely determined by husk growth. Transcription regulator factors are responsible for enhancing cell growth in the maternal ovule, resulting in seed growth. Phytohormones induce significant effects on entire features of growth and development of plants and also regulate seed size. Moreover, the vegetative parts are the major source of nutrients, including the majority of carbon and nitrogen-containing molecules for the reproductive part to control seed size. There is a need to increase the size of seeds without affecting the number of seeds in plants through conventional breeding programs to improve grain yield. In the past decades, many important genetic factors affecting seed size and yield have been identified and studied. These important factors constitute dynamic regulatory networks governing the seed size in response to environmental stimuli. In this review, we summarized recent advances regarding the molecular factors regulating seed size in Arabidopsis and other crops, followed by discussions on strategies to comprehend crops' genetic and molecular aspects in balancing seed size and yield.

MiR-1246 is implicated as a possible candidate for endometrium remodelling facilitating implantation in buffalo (Bubalus bubalis).

The microRNAs (miRs) secreted by the trophectoderm (TE) cells have recently been implicated in the conceptus-endometrial cross talk during implantation and placentation. These miRs modulate various cellular processes during conception and throughout the pregnancy by regulating the gene expression in the foetal and maternal tissues. This study was undertaken to elucidate the function of TE secreted miRNAs in the maternal-foetal cross-talk during implantation/placentation in buffalo. The in vitro produced blastocysts were cultured on a cumulus feeder layer for 21 days. The relative expression profiles of a selected panel of miRs was generated using the spent media collected on Days 0, 7, 12, 16, and 21. A custom-designed mirVana™ miRNA mimic was used to transfect the endometrial epithelial cells (EECs) in order to determine the role of miRNA exhibiting highest expression on Days 21 and 21. The expression of miR-1246 (p < 0.001) and let-7b (p < 0.01) was found to be significantly higher on Day 21 of TE culture in comparison to the control (Day 0). This elevated expression indicated the involvement of these miRs in the maternal-foetal cross-talk. Interestingly, after the transfection of EECs with miRNA mimic for miR-1246 (a novel molecule vis-à-vis implantation), the expression of beta-catenin and mucin1 in these cells was found to be significantly (p < 0.05) downregulated vis-à-vis the control, that is, the IFN-τ primed EECs (before transfection). The TE secreted miR-1246 appeared to lower the expression of the endometrial receptivity genes (mucin1 and beta-catenin) which apparently assists the endometrium in preparing for placentation.

PSIII-1 Late-Breaking: Fighting Fetal Morbidity at the Fetal-Maternal Interface One Chemokine Access at a Time

Abstract Improper placentation is the root cause to intrauterine growth restriction (IUGR) and fetal mortality in livestock. This study aims to further characterize the importance of the C-X-C motif chemokine receptor 4 (CXCR4) and its ligand CXCL12 on placentation and fetal growth through potential impacts on the insulin-like growth factors (IGF) and their binding proteins (IGFBP1-3). CXCR4 and CXCL12 are implicated in placentation though the exact roles are unclear. The peptides insulin-like growth factors 1 and 2 have impacts on fetal growth, placental development, and trophoblast differentiation and if the IGFs are down regulated, a corresponding decrease in placenta and fetus size has been observed. The roles of the IGFs and their binding proteins in disease states like IUGR are not completely known but studies have demonstrated them to be contributing factors. Using an in-vivo sheep model we surgically inserted osmotic pumps on day 12 (d12) of gestation ipsilateral to the corpus luteum to deliver treatments into the uterus of bred ewes. Pumps delivered either saline (control) or AMD3100, the CXCR4 inhibitor at a 1x, 1.5x, or 3x dose into the uterine lumen over the course of 14 days. Our objective was to determine if disrupting the CXCL12/CXCR4 axis during implantation alters the expression of IGFs and their binding proteins in the placenta at mid and late gestation. At midgestation (d90) and late gestation (d135) placental and fetal samples were obtained for analysis. Of the targets tested, mRNA expression was significantly decreased by AMD3100 treatment for both IGF-1 (P = 0.05) and IGF-2 (P = 0.02) compared to control primarily in maternal placenta tissues on d135. For fetal tissue samples, d90 mRNA expression for IGF-1 (P = 0.04) IGFBP-2 (P = 0.02) and IGFBP-3 (P = 0.03) increased in the 3x AMD3100 treated group compared to the control while in d135 samples, IGF-1was significantly decreased (P = 0.04) by the 1x treatments compared to control. Our preliminary data show an importance of the CXCL12- CXCR4 signaling on placentation and that impairment of this axis may alter IGFs in multiple tissue types later in gestation. Insights into this chemokine axis will lead to a greater understanding of placental development and its importance to the health of mother and offspring.

PS-2 Early Intrauterine Suppression of CXCL12-CXCR4 Alters Expression of Placental Inflammatory Profile at Mid-to-Late Gestation

Abstract A proper balance of inflammatory cytokines at the fetal-maternal interface is crucial for successful embryo implantation and placental formation. Chemokine ligand 12 (CXCL12) and receptor CXCR4 are expressed by fetal and maternal placental tissues and implicated in cytokine synthesis. However, mechanisms controlling the axis and placental inflammatory profile are not well characterized. Using an in-vivo sheep model, we previously demonstrated suppressing CXCL12-CXCR4 signaling at the fetal-maternal interface during implantation yielded dysregulated production of inflammatory cytokines in the placenta. Our objective was to determine if disrupting the cytokine profile during implantation alters the placental inflammatory profile at mid-to-late gestation. Day 12 post-breeding, osmotic pumps were surgically installed in 37 ewes to deliver CXCR4 inhibitor (1.5X dose, n = 8; 1X dose, n = 8; 3X dose, n = 8) or saline (n = 13) into the uterine lumen ipsilateral to the corpus luteum for 14 days. On days 90 and 135 of gestation, placental tissues were collected; maternal (caruncle) and fetal (cotyledon) placenta components were then separated and analyzed. Real-time qPCR was used to measure gene expression of pro-inflammatory cytokines tumor necrosis factor (TNF), interferon-γ (IFNγ), interleukin-12 (IL12), and anti-inflammatory cytokines interleukin-10 (IL10) and transforming growth factor-β (TGFβ). Gene expression for TGFβ from tissues ipsilateral to the pump on day 90 increased (P &amp;lt; 0.03) in caruncles from 3x treated ewes compared to control ewes while IL10 mRNA decreased (P &amp;lt; 0.02) in cotyledons from 1.5x compared to 3x treatment. Furthermore, analysis of day 135 1x treated ewes showed greater expression (P &amp;lt; 0.03) of IL12 in caruncles ipsilateral compared to contralateral of the pump; meanwhile IL10 showed decreased expression (P &amp;lt; 0.02) in cotyledons ipsilateral compared to contralateral of the pump. High levels of TGFβ, IFNγ (whose production is promoted by increased IL12), and TNF along with decreased levels of IL10 have been associated with preeclampsia in women. The changes in gene expressions of ovine immune cytokines with a disrupted CXCL12-CCR4 axis may be related to preeclamptic events. Ultimately, modulating CXCL12-induced actions is a novel approach to manipulating the fetal-maternal environment when most pregnancy losses occur and may reveal methods to improve reproductive success and fetal health in livestock.

Developmental and mechanical roles of Reichert's membrane in mouse embryos.

Embryonic development and growth in placental mammals proceeds in utero with the support of exchanges of gases, nutrients and waste products between maternal tissues and offspring. Murine embryos are surrounded by several extraembryonic membranes, parietal and visceral yolk sacs, and amnion in the uterus. Notably, the parietal yolk sac is the most outer membrane, consists of three layers, trophoblasts and parietal endoderm (PaE) cells, and is separated by a thick basal lamina termed Reichert's membrane (RM). RM is composed of extracellular matrix (ECM) initially formed as the basement membrane of the trophectoderm of pre-implanted embryos and followed by the heavy deposition of ECM mainly produced in PaE cells of post-implanted embryos. In addition to the physiological roles of RM, such as gas and nutrient exchange, it also plays a crucial role in cushioning and dispersing intrauterine pressures exerted on embryos for normal egg-cylinder morphogenesis. Mechanistically, such intrauterine pressures generated by uterine smooth muscle contractions appear to be involved in the elongation of the egg-cylinder shape, along with primary axis formation, as an important biomechanical element in utero. This review focuses on our current views of the roles of RM in properly buffering intrauterine mechanical forces for mouse egg-cylinder morphogenesis. This article is part of the theme issue 'Extraembryonic tissues: exploring concepts, definitions and functions across the animal kingdom'.

Spontaneous preterm birth: Involvement of multiple feto-maternal tissues and organ systems, differing mechanisms, and pathways.

Survivors of preterm birth struggle with multitudes of disabilities due to improper in utero programming of various tissues and organ systems contributing to adult-onset diseases at a very early stage of their lives. Therefore, the persistent rates of low birth weight (birth weight < 2,500 grams), as well as rates of neonatal and maternal morbidities and mortalities, need to be addressed. Active research throughout the years has provided us with multiple theories regarding the risk factors, initiators, biomarkers, and clinical manifestations of spontaneous preterm birth. Fetal organs, like the placenta and fetal membranes, and maternal tissues and organs, like the decidua, myometrium, and cervix, have all been shown to uniquely respond to specific exogenous or endogenous risk factors. These uniquely contribute to dynamic changes at the molecular and cellular levels to effect preterm labor pathways leading to delivery. Multiple intervention targets in these different tissues and organs have been successfully tested in preclinical trials to reduce the individual impacts on promoting preterm birth. However, these preclinical trial data have not been effectively translated into developing biomarkers of high-risk individuals for an early diagnosis of the disease. This becomes more evident when examining the current global rate of preterm birth, which remains staggeringly high despite years of research. We postulate that studying each tissue and organ in silos, as how the majority of research has been conducted in the past years, is unlikely to address the network interaction between various systems leading to a synchronized activity during either term or preterm labor and delivery. To address current limitations, this review proposes an integrated approach to studying various tissues and organs involved in the maintenance of normal pregnancy, promotion of normal parturition, and more importantly, contributions towards preterm birth. We also stress the need for biological models that allows for concomitant observation and analysis of interactions, rather than focusing on these tissues and organ in silos.

Fetal muscle extract improves muscle function and performance in aged mice.

Background: Loss of skeletal muscle mass and function is one of the major musculoskeletal health problems in the aging population. Recent studies have demonstrated differential proteomic profiles at different fetal stages, which might be associated with muscle growth and development. We hypothesized that extract derived from fetal muscle tissues at the stage of hypertrophy could ameliorate the loss of muscle mass and strength in aged mice. Methods: To allow sufficient raw materials for investigation, skeletal muscle extract from fetal sheep at week 16 of gestation and maternal tissue were used in the present study. iTRAQ (isobaric tags for relative and absolute quantitation) and KEGG pathway analyses identified differentially expressed proteins in fetal sheep muscle extract vs. adult sheep muscle extract. Effects of FSME and ASME on human myoblast proliferation were studied. To examine the effect of FSME in vivo, C57BL/6 male mice at 20 months of age were subjected to intramuscular administration of FSME or vehicle control for 8 weeks. A grip strength test and ex vivo muscle force frequency test were conducted. Finally, serum samples were collected for multiplex analysis to determine potential changes in immunological cytokines upon FSME injection. Results: Compared with ASME, 697 and 412 peptides were upregulated and downregulated, respectively, in FSME, as indicated by iTRAQ analysis. These peptides were highly related to muscle development, function, and differentiation from GO enrichment analysis. FSME promoted cell proliferation of myoblast cells (+300%, p < 0.01) without causing significant cytotoxicity at the tested concentration range compared with ASME. After 8 weeks of FSME treatment, the percentage of lean mass (+10%, p < 0.05), grip strength (+50%, p < 0.01), and ability in fatigue resistance were significantly higher than those of the control group. Isometric forces stimulated by different frequencies were higher in the control group. Histologically, the control group showed a larger cross-sectional area (+20%, p < 0.01) than the FSME group. The multiplex assay indicated that FSME treatment did not lead to an elevated circulatory level of inflammatory cytokines. Of note, after FSME treatment, we observed a significant drop in the circulating level of IL-12 (p40) from 90.8 ± 48.3 pg/ml to 82.65 ± 4.4 pg/ml, G-CSF from 23476 ± 8341.9 pg/ml to 28.35 ± 24.2 pg/ml, KC from 97.09 ± 21.2 pg/ml to 29.2 ± 7.2 pg/ml, and RANTES from 325.4 ± 17.3 pg/ml to 49.96 ± 32.1 pg/ml. Conclusion: This is the first study demonstrating the beneficial effect of fetal muscle extract on muscle health in aged mice. Further analysis of the active ingredients of the extract will shed light on the development of a novel treatment for sarcopenia.

Embryonic growth retardation and altered expression of IGF-II is reciprocal induced by phytocompounds during early gestation in mice

Methanolic crude extract of Scoparia dulcis (CESD) was orally administered to female mice during the early gestation (day 4–day 8) at a dose of 500 mg/kg/day. It induces embryo resorption and morphological changes of fetal maternal tissue. Histomorphology was studied by routine hematoxylin eosin stain. In situ immunofluorescence localization of IGF-II using Texas red showed an ordered expression of the growth factor in the maternal decidual cells, trophoblast cells and the embryo. Western blot analysis showed a gradual increase of IGF-II from D4 to D8 of control females. In contrast, the CESD-treated females showed resorption of embryo on D8 with disorganized in situ expression and lowered IGF-II in fetal maternal tissue. The phytocompounds present in the CESD could modulate either the ER or IGF-II receptors causing reduced IGF-II expression in the target tissues which lead to the failure of embryonic growth during periimplantation.

MATERNAL FIBROID IMPACT ON CELL FREE DNA (cfDNA) SCREENING

In cell free DNA (cfDNA) screening, a proportion of the circulating cfDNA is placental and serves as a proxy for fetal aneuploidy status. As the remaining cfDNA originates from maternal tissue, identification of unexpected maternal findings is possible. Like other tissues, fibroids can contribute cfDNA fragments to maternal plasma. ∼50% of fibroids have abnormal chromosome complements which may confound fetal aneuploidy screening.1-3 Here we investigate cfDNA data and results from 57 patients with known fibroids.

Loss of function of the maternal membrane oestrogen receptor ERα alters expansion of trophoblast cells and impacts mouse fertility.

The binding of 17β-oestradiol to oestrogen receptor alpha (ERα) plays a crucial role in the control of reproduction, acting through both nuclear and membrane-initiated signalling. To study the physiological role of membrane ERα in the reproductive system, we used the C451A-ERα mouse model with selective loss of function of membrane ERα. Despite C451A-ERα mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do become pregnant, allowing the investigation of the role of ERα during pregnancy for the first time. All neonatal deaths of the mutant offspring mice resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERα females exhibited partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality resulted from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells into the utero-placental unit, which is associated with an imbalance in expression of angiogenic factors. Together, these processes control the trophoblast-mediated spiral arterial remodelling. Hence, loss of membrane ERα within maternal tissues clearly alters the activity of invasive trophoblast cells during placentogenesis. This previously unreported function of membrane ERα could open new avenues towards a better understanding of human pregnancy-associated pathologies.

Placental Vitamin D Metabolism as Well as its Relations to Circulating Vitamin D Metabolites in Pregnancies

Background: Uncertainty exists about the impact of placental vit D metabolism on mother's blood levels of vit D in people. Objective: Awareness of placental vit D metabolism and how it affects the amount of vit D metabolites in mother's blood was one of the goals of this investigation. Methods: To take part in a 14-week controlled feeding experiment, 27 third-trimester singleton pregnant women in good health from Hayatabad Medical Complex during Jan 2022 to April 2022. Female trophoblasts in vitro were further treated using Vitamin D3-13C to investigate the synthesis of vit D intermediates. Results: In maternal tissue, there was a substantial connection between 24,25-Dihydroxycholecalciferol and 25-hydroxyvitamin D. These placental metabolites were also closely connected to the corresponding compounds found in maternal circulation. 3-epi-25-Hydroxyvitamin D3 and low density lipoprotein-related protein 2 with 25-hydroxyvitamin D; CYP2R1 with 3-epi-25-Hydroxyvitamin D3; Cubilin (CUBN) with 25-hydroxyvitamin D; CYP27B1 with 3-epi-25-Hydroxyvitamin D3 and 1,25-dihydroxyvitamin D and CYP24A1 with 25-hydroxyvitamin D, 24,25-Dihydroxycholecalciferol all showed positive relationships. Conclusion: Strong relationships between the levels of circulating vit D metabolites in pregnancy and a number of placental markers of vit D metabolism suggest the hypothesis that the profile of vit D metabolites in mother's blood is altered by the placenta. Keywords: 24,25-Dihydroxycholecalciferol (24,25(OH)2D3), 25-hydroxyvitamin D (25(OH)D3), 3-epi-25-Hydroxyvitamin D3 (epi-25(OH)D3), CYP2R1, CYP24A1

A NAC-EXPANSIN module enhances maize kernel size by controlling nucellus elimination

Maize early endosperm development is initiated in coordination with elimination of maternal nucellar tissues. However, the underlying mechanisms are largely unknown. Here, we characterize a major quantitative trait locus for maize kernel size and weight that encodes an EXPANSIN gene, ZmEXPB15. The encoded β-expansin protein is expressed specifically in nucellus, and positively controls kernel size and weight by promoting nucellus elimination. We further show that two nucellus-enriched transcription factors (TFs), ZmNAC11 and ZmNAC29, activate ZmEXPB15 expression. Accordingly, these two TFs also promote kernel size and weight through nucellus elimination regulation, and genetic analyses support their interaction with ZmEXPB15. Importantly, hybrids derived from a ZmEXPB15 overexpression line have increased kernel weight, demonstrates its potential value in breeding. Together, we reveal a pathway modulating the cellular processes of maternal nucellus elimination and early endosperm development, and an approach to improve kernel weight.

ТHE METABOLIC ASPECTS OF PREECLAMPSIA DEVELOPMENT

Complications associated with preeclampsia (PE) include fetal growth retardation, premature birth, prenatal and postpartum hemorrhage, perinatal loss, and more. Obese women have an increased risk of developing PE, probably due to impaired placental development due to altered metabolic homeostasis. The aim was to generalize current knowledge about the role of risk factors associated with obesity and hypercholesterolemia in PE with an emphasis on the results of preclinical models. Material and methods. In reviewing the literature, we used Medline systems from PubMed (2011). The search was adapted for Embase (2014-2022) and Scopus (2015-2022). The inclusion criteria were: the effect of obesity on pregnancy; experimental models of the pathogenesis of obesity during pregnancy; the features of predictive diagnosis of obese women at the stage of preconception and during pregnancy; features of antenatal care in obese women. The study was performed at Vinnytsya National Pirogov Memorial Medical University, according to research work № 0121U109141 “Optimization of early diagnosis and preventive treatment of perinatal complications caused by gestational endotheliopathy.” Results. Inflammatory cytokines from maternal adipose tissue and hypercholesterolemia have been associated with systemic inflammation, hypertension, and other adverse effects associated with PE. The main pathways of the negative influence of obesity on the genesis of PE were realized due to the manifested gestational endotheliopathy. Decreases in adipose tissue and associated adipokines were associated with optimization of placental angiogenesis and an overall improvement in the adverse effects associated with PE. Conclusions. Increased maternal adipose tissue mass and cholesterol levels contribute to metabolic disorders and systemic inflammation, which may contribute to the development of gestational endotheliopathy and subsequent abnormal placenta vascularization. Further research will need to further clarify the contribution of pharmacotherapy, as well as some lifestyle adjustments, including preconceptional weight loss and the results of PE in women at high risk of obesity.

PSII-A-11 Suppressing the Cxcl12-Cxcr4 Chemokine Axis at the Fetal-Maternal Interface During Implantation Results in Altered Expression of Inflammatory Cytokines in Ovine Placenta at Midgestation

Abstract A proper balance of pro and anti-inflammatory cytokines at the fetal-maternal interface is crucial for successful embryo implantation and placental formation (placentation) during early gestation. However, mechanisms controlling this inflammatory profile are not well characterized. The C-X-C motif chemokine ligand 12 (CXCL12) and its receptor CXCR4 are expressed by fetal and maternal placental tissues and implicated in cytokine synthesis; roles of this axis during placentation are unclear. Using an in vivo sheep model, we demonstrated that suppressing CXCL12-CXCR4 signaling at the fetal-maternal interface during implantation results in dysregulated production of inflammatory cytokines in the placenta. The objective of the current study was to determine if the disrupted cytokine profile from suppressing CXCL12-CXCR4 signaling early in gestation would result in altered placental inflammatory profile at midgestation. On day 12 post-breeding, osmotic pumps were surgically installed in 37 ewes and delivered either CXCR4 inhibitor (AMD3100) at 1X dose, (n=8), 1.5X, (n=8), or 3X, (n=8) or saline (n=13) into the uterine lumen ipsilateral to the corpus luteum for 14 days. On days 90 and 135, placental tissues were collected, and maternal and fetal placenta components separated and analyzed. Gene expression for select cytokines were analyzed in the placenta using Real-time qPCR. On day 90, mRNA expression was significantly altered by AMD3100 treatment for tumor necrosis factor (TNF), interleukin 12 (IL-12), and transforming growth factor beta (TGFB) in fetal placenta. Expression of TGFB in fetal placenta was also altered by AMD3100 treatment compared to control on day 135 whereas IL-12 expression was significantly altered in maternal placenta on day 135. In conclusion, modulating CXCL12-induced actions is a novel approach to manipulating the fetal-maternal environment when most pregnancy losses occur. Increasing our understanding of CXCL12-induced actions controlling the placental inflammatory environment will hopefully reveal methods to improve reproductive success and fetal health in livestock.

Role of MicroRNAs in Cardiac Disease with Stroke in Pregnancy.

Pregnancy-related cardiovascular disease with stroke remains a considerable source of higher maternal morbidity and mortality occurs in periods of pregnancy, delivery, and postpartum. It is essential to counsel the mother before pregnancy by an expert cardiologist and obstetric team to discuss any event related to preexistent cardiac or past preeclampsia for estimation of maternal and fetal risks. In pregnancy, the cardiac state includes hypertensive disorders, ischemic heart disease, valvular disease, and postpartum stroke. The incidence of stroke is increasing in pregnancy, particularly in postpartum, and its strong relationship with hypertensive disorders of pregnancy (preeclampsia). The combined cardiologist and obstetrics team requires during pregnancy mainly due to the approach to the management of a cardiac disease that subsequently prevents stroke postpartum. Therefore, a general perception of cardiac disease during pregnancy, delivery, and postpartum should be a core knowledge extent for all cardiovascular and clinicians. Many studies provided linked that deregulation of microRNAs (miRNAs) in maternal circulation and placenta tissue may development of pregnancy complications including preeclampsia considered a diagnostic marker. The desire of this review provides a detailed outline of current knowledge and dealing in this field with strength on the physiological changes during pregnancy.

Negative regulation of seed germination by maternal AFB1 and AFB5 in Arabidopsis.

The plant hormone auxin suppresses seed germination, but how auxin does it remains poorly understood. While studying the functions of the AUXIN SIGNALING F-BOX (AFB) auxin co-receptors in Arabidopsis, we consistently isolated AFB1 and AFB5 in reproductive tissues in co-immunoprecipitation experiments using their interacting protein ASK1 as the bait. However, T2 seeds of the AFB1 or AFB5 transgenic lines generated for the co-immunoprecipitation experiments frequently failed to germinate, which led to the studies of seed germination in these plants and afb1 and afb5 mutants, and AFB1 and AFB5 expression in nearly mature fruit and imbibed seeds using AFB1:GUS and AFB5:GUS lines. We found that AFB1 and AFB5 acted in maternal tissues to suppress seed germination and their effects were positively correlated with the plants’ sensitivity to indole acetic acid. Conversely, afb1 and afb5 single mutants exhibited faster seed germination than the wild type and the seeds of the afb1-5afb5-5 double mutant germinated even faster than those of the afb1-5 and afb5-5 single mutants. Seed germination of the afb1-5afb5-5 double mutant also exhibited higher sensitivity to gibberellic acid than that of the wild-type and the afb1-3, afb1-5 and afb5-5 single mutants. Both AFB1 and AFB5 were expressed in the funiculus during seed maturation, and AFB1 was also transiently expressed in a small chalazal region surrounding the hilum in the seed coat during seed imbibition. Therefore, AFB1 and AFB5 likely suppress seed germination in the funiculus and AFB1 also briefly suppresses seed germination in the chalaza during seed imbibition.

Progesterone Receptor Modulates Extraembryonic Mesoderm and Cardiac Progenitor Specification during Mouse Gastrulation.

Progesterone treatment is commonly employed to promote and support pregnancy. While maternal tissues are the main progesterone targets in humans and mice, its receptor (PGR) is expressed in the murine embryo, questioning its function during embryonic development. Progesterone has been previously associated with murine blastocyst development. Whether it contributes to lineage specification is largely unknown. Gastrulation initiates lineage specification and generation of the progenitors contributing to all organs. Cells passing through the primitive streak (PS) will give rise to the mesoderm and endoderm. Cells emerging posteriorly will form the extraembryonic mesodermal tissues supporting embryonic growth. Cells arising anteriorly will contribute to the embryonic heart in two sets of distinct progenitors, first (FHF) and second heart field (SHF). We found that PGR is expressed in a posterior–anterior gradient in the PS of gastrulating embryos. We established in vitro differentiation systems inducing posterior (extraembryonic) and anterior (cardiac) mesoderm to unravel PGR function. We discovered that PGR specifically modulates extraembryonic and cardiac mesoderm. Overexpression experiments revealed that PGR safeguards cardiac differentiation, blocking premature SHF progenitor specification and sustaining the FHF progenitor pool. This role of PGR in heart development indicates that progesterone administration should be closely monitored in potential early-pregnancy patients undergoing infertility treatment.

Study on exogenous application of thidiazuron on seed size of Brassica napus L.

Thidiazuron (TDZ) is a novel and efficient cytokinin commonly used in tissue culture, and numerous studies have demonstrated that TDZ can increase berry size. However, no study to date has explored the effect of TDZ on seed size of Brassica napus and the mechanism. To shed light on the effect of TDZ on the seed size of B. napus, four different concentrations of TDZ were applied to B. napus. Results indicated that TDZ treatment could increase the seed diameter and silique length of B. napus to varying degrees and 100 and 200 μmol/L TDZ treatments were the most effective with a 3.6 and 4.6% increase in seed diameter, respectively. In addition, the yield of B. napus was also substantially increased under TDZ treatment. On the other hand, confocal micrographs of embryos and cotyledon cells suggested that embryos and their cotyledon epidermal cells treated with 200 μmol/L TDZ were obviously larger in size than the control. Furthermore, TDZ promoted the upregulation of some key maternal tissue growth-related genes, including two G-protein signaling genes (AGG3 and RGA1) and two transcriptional regulators (ANT and GS2). The expression analysis of genes related to the auxin metabolic pathways, G-protein signaling, endosperm growth and transcriptional regulators confirmed that treatment with TDZ negatively regulated the key genes ABI5, AGB1, AP2, ARF2, and ARF18 during bud development stage and florescence. The results strongly suggested that TDZ might regulate the transcriptional levels of key genes involved in auxin metabolic pathways, G-protein signaling, endosperm growth and transcriptional regulators, which resulted in bigger cotyledon epidermal cells and seed size in B. napus. This study explored the mechanism of TDZ treatment on the seed size of B. napus and provided an important reference for improving rapeseed yield.