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Fetal gene expression

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https://www.readbyqxmd.com/read/28822817/rosiglitazone-promotes-cardiac-hypertrophy-and-alters-chromatin-remodeling-in-isolated-cardiomyocytes
#1
Lama Fawaz Pharaon, Naglaa Fathi El-Orabi, Muhammad Kunhi, Nadya Al Yacoub, Salma Mahmoud Awad, Coralie Poizat
Rosiglitazone is an anti-diabetic agent that raised a major controversy over its cardiovascular adverse effects. There is in vivo evidence that Rosiglitazone promotes cardiac hypertrophy by PPAR -γ-independent mechanisms. However, whether Rosiglitazone directly alters hypertrophic growth in cardiac cells is unknown. Chromatin remodeling by histone post-translational modifications has emerged as critical for many cardiomyopathies. Based on these observations, this study was initiated to investigate the cardiac hypertrophic effect of Rosiglitazone in a cellular model of primary neonatal rat cardiomyocytes (NRCM)...
August 16, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28821329/cardiac-progenitor-cell-recruitment-drives-fetal-cardiac-regeneration-by-enhanced-angiogenesis
#2
Carlos Zgheib, Maggie M Hodges, Myron W Allukian, Junwang Xu, Kara L Spiller, Joseph H Gorman, Robert C Gorman, Kenneth W Liechty
BACKGROUND: In contrast to adults, the fetal response to myocardial infarction (MI) is regenerative, requiring the recruitment of cardiac progenitor cells to replace infarcted myocardium. Macrophage contribution to tissue repair depends on their phenotype: M1 are proinflammatory and initiate angiogenesis; M2a are profibrotic and contribute to blood vessels maturation; and M2c are proremodeling and proangiogenesis. The goal of the present study was to expand on this work by examining cardiac progenitor cells recruitment, and the role of macrophages in promoting angiogenesis and cardiac regeneration in the fetal heart after MI...
August 16, 2017: Annals of Thoracic Surgery
https://www.readbyqxmd.com/read/28821223/maternal-nutrient-restriction-in-mid-to-late-gestation-influences-fetal-mrna-expression-in-muscle-tissues-in-beef-cattle
#3
Francois Paradis, Katie M Wood, Kendall C Swanson, Stephen P Miller, Brian W McBride, Carolyn Fitzsimmons
BACKGROUND: Manipulating maternal nutrition during specific periods of gestation can result in re-programming of fetal and post-natal development. In this experiment we investigated how a feed restriction of 85% compared with 140% of total metabolizable energy requirements, fed to cows during mid-to-late gestation, influences phenotypic development of fetuses and mRNA expression of growth (Insulin-Like Growth Factor family and Insulin Receptor (INSR)), myogenic (Myogenic Differentiation 1 (MYOD1), Myogenin (MYOG), Myocyte Enhancer Factor 2A (MEF2A), Serum Response Factor (SRF)) and adipogenic (Peroxisome Proliferator Activated Receptor Gamma (PPARG)) genes in fetal longissimus dorsi (LD) and semitendinosus (ST) muscle...
August 18, 2017: BMC Genomics
https://www.readbyqxmd.com/read/28820906/exposure-to-fine-particulate-matter-in-the-air-alters-placental-structure-and-the-renin-angiotensin-system
#4
Sônia de Fátima Soto, Juliana Oliveira de Melo, Guilherme D'Aprile Marchesi, Karen Lucasechi Lopes, Mariana Matera Veras, Ivone Braga de Oliveira, Regiane Machado de Souza, Isac de Castro, Luzia Naôko Shinohara Furukawa, Paulo Hilário Nascimento Saldiva, Joel C Heimann
METHODS: Female Wistar rats were exposed to filtered air (F) or to concentrated fine particulate matter (P) for 15 days. After mating, the rats were divided into four groups and again exposed to F or P (FF, FP, PF, PP) beginning on day 6 of pregnancy. At embryonic day 19, the placenta was collected. The placental structure, the protein and gene expression of TGFβ1, VEGF-A, and its receptor Flk-1 and RAS were evaluated by indirect ELISA and quantitative real-time PCR. RESULTS: Exposure to P decreased the placental mass, size, and surface area as well as the TGFβ1, VEGF-A and Flk-1 content...
2017: PloS One
https://www.readbyqxmd.com/read/28820499/choline-supplementation-normalizes-fetal-adiposity-and-reduces-lipogenic-gene-expression-in-a-mouse-model-of-maternal-obesity
#5
Chauntelle Jack-Roberts, Yaelle Joselit, Khatia Nanobashvili, Rachel Bretter, Olga V Malysheva, Marie A Caudill, Anjana Saxena, Kathleen Axen, Ahmed Gomaa, Xinyin Jiang
Maternal obesity increases fetal adiposity which may adversely affect metabolic health of the offspring. Choline regulates lipid metabolism and thus may influence adiposity. This study investigates the effect of maternal choline supplementation on fetal adiposity in a mouse model of maternal obesity. C57BL/6J mice were fed either a high-fat (HF) diet or a control (NF) diet and received either 25 mM choline supplemented (CS) or control untreated (CO) drinking water for 6 weeks before timed-mating and throughout gestation...
August 18, 2017: Nutrients
https://www.readbyqxmd.com/read/28816640/exosomal-microrna-communication-between-tissues-during-organogenesis
#6
Toru Hayashi, Matthew P Hoffman
Epithelial-mesenchymal interactions are required to coordinate cell proliferation, patterning, and functional differentiation of multiple cell types in a developing organ. This exquisite coordination is dependent on various secreted molecules that provide developmental signals to mediate these tissue interactions. Recently, it was reported that mature mesenchymal-derived microRNAs (miRNAs) in the fetal mouse salivary gland are loaded into exosomes, and transported to the epithelium where they influence progenitor cell proliferation...
August 17, 2017: RNA Biology
https://www.readbyqxmd.com/read/28816360/c-c-motif-chemokine-ligand-2-regulates-lps-induced-inflammation-and-er-stress-to-enhance-proliferation-of-bovine-endometrial-epithelial-cells
#7
Whasun Lim, Hyocheol Bae, Fuller W Bazer, Sung-Man Kim, Gwonhwa Song
Chemokines play an important role in regulating the complex immune system at the maternal-fetal interface during pregnancy. Among various chemokines, C-C motif chemokine ligand 2 (CCL2) plays a role in the recruitment of immune regulatory cells to implantation sites within the endometrium. In cattle, CCL2 is abundantly expressed in the uterine endometrium. However, its intracellular signaling has not been identified. In this study, we examined the effects of CCL2 on bovine endometrial (BEND) cell proliferation...
August 17, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28814758/targeted-insertion-of-an-anti-cd2-monoclonal-antibody-transgene-into-the-ggta1-locus-in-pigs-using-foki-dcas9
#8
Mark B Nottle, Evelyn J Salvaris, Nella Fisicaro, Stephen McIlfatrick, Ivan Vassiliev, Wayne J Hawthorne, Philip J O'Connell, Jamie L Brady, Andrew M Lew, Peter J Cowan
Xenotransplantation from pigs has been advocated as a solution to the perennial shortage of donated human organs and tissues. CRISPR/Cas9 has facilitated the silencing of genes in donor pigs that contribute to xenograft rejection. However, the generation of modified pigs using second-generation nucleases with much lower off-target mutation rates than Cas9, such as FokI-dCas9, has not been reported. Furthermore, there have been no reports on the use of CRISPR to knock protective transgenes into detrimental porcine genes...
August 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28814477/iodine-excess-exposure-during-pregnancy-and-lactation-impairs-maternal-thyroid-function-in-rats
#9
Caroline Serrano-Nascimento, Rafael Salgueiro, Kaio Vitzel, Thiago Urgal Pantaleao, Vania Maria Correa da Costa, Maria Tereza Nunes
Adequate maternal iodine consumption during pregnancy and lactation guarantees normal thyroid hormones (TH) production, which is crucial to the development of the fetus. Indeed, iodine deficiency is clearly related to maternal hypothyroidism and deleterious effects in the fetal development. Conversely, the effects of iodine excess (IE) consumption on maternal thyroid function are still controversial. Therefore, this study aimed to investigate the impact of IE exposure during pregnancy and lactation periods on maternal hypothalamus-pituitary-thyroid axis...
August 16, 2017: Endocrine Connections
https://www.readbyqxmd.com/read/28813466/comprehensive-comparison-of-neonate-and-adult-human-platelet-transcriptomes
#10
Eva Caparrós-Pérez, Raúl Teruel-Montoya, Mª José López-Andreo, Mª Carmen Llanos, José Rivera, Verónica Palma-Barqueros, Jose E Blanco, Vicente Vicente, Constantino Martínez, Francisca Ferrer-Marín
Understanding the underlying mechanisms of the well-substantiated platelet hyporeactivity in neonates is of interest given their implications for the clinical management of newborns, a population at higher bleeding risk than adults (especially sick and preterm infants), as well as for gaining insight into the regulatory mechanisms of platelet biology. Transcriptome analysis is useful in identifying mRNA signatures affecting platelet function. However, human fetal/neonatal platelet transcriptome analysis has never before been reported...
2017: PloS One
https://www.readbyqxmd.com/read/28811181/beneficial-effects-of-postnatal-choline-supplementation-on-long-term-neurocognitive-deficit-resulting-from-fetal-neonatal-iron-deficiency
#11
Bruce C Kennedy, Phu V Tran, Maulika Kohli, Jamie J Maertens, Jonathan C Gewirtz, Michael K Georgieff
Early-life iron deficiency is a common nutrient condition worldwide and can result in cognitive impairment in adulthood despite iron treatment. In rodents, prenatal choline supplementation can diminish long-term hippocampal gene dysregulation and neurocognitive deficits caused by iron deficiency. Since fetal iron status is generally unknown in humans, we determined whether postnatal choline supplementation exerts similar beneficial effects. Male rat pups were made iron deficient (ID) by providing pregnant and nursing dams an ID diet (3-6ppm Fe) from gestational day (G) 3 through postnatal day (P) 7, and an iron-sufficient (IS) diet (200ppm Fe) thereafter...
August 12, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28807863/prenatal-diagnosis-of-complex-phenotype-in-a-13-week-old-fetus-with-an-interstitial-multigene-deletion-20q13-13-q13-2-by-chromosomal-microarray
#12
Feodora Stipoljev, Danka Miric-Tesanic, Tomislav Hafner, Maja Barbalic, Monika Logara, Ruzica Lasan-Trcic, Ana Vicic, Romana Gjergja-Juraski
We report the first trimester three-dimensional ultrasonographic findings in a 13-week-old fetus with complex phenotype and a de novo 4.7 Mb multigene deletion encompassing chromosome region 20q13.13-q13.2 detected by chromosomal microarray. Fetal sonography detected radial-ray anomalies in the form of bilateral absence of thumbs and the left club hand deformity. The presence of single atrioventricular canal instead of the atrial septal defect typical for Holt-Oram syndrome pointed us to rather suspect the SALL4 related diseases...
August 11, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/28807280/immunization-with-inactivated-antigens-of-neospora-caninum-induces-toll-like-receptors-3-7-8-and-9-in-maternal-fetal-interface-of-infected-pregnant-heifers
#13
M S Marin, Y P Hecker, S Quintana, S E Pérez, M R Leunda, G J Cantón, E R Cobo, D P Moore, A C Odeón
Neospora caninum is an obligate parasite and a major cause of abortion in cattle. Pregnancy failures appear to be associated with weak innate defences on the maternal-fetal interface during infection with N. caninum. Herein, we studied the gene expression of Toll-like receptors (TLRs) in pregnant heifers immunized with different vaccine formulations against N. caninum before mating and then challenged the heifers with live N. caninum on day 70 of gestation. TLR7 and TLR8 expression was upregulated in the placental caruncle of infected-pregnant heifers previously exposed to live N...
August 30, 2017: Veterinary Parasitology
https://www.readbyqxmd.com/read/28804622/human-placental-growth-hormone-in-normal-and-abnormal-fetal-growth
#14
Alexandros Velegrakis, Maria Sfakiotaki, Stavros Sifakis
Human placental growth hormone (PGH), encoded by the growth hormone (GH) variant gene on chromosome 17, is expressed in the syncytiotrophoblast and extravillous cytotrophoblast layers of the human placenta. Its maternal serum levels increase throughout pregnancy, and gradually replaces the pulsatile secreted pituitary GH. PGH is also detectable in cord blood and in the amniotic fluid. This placental-origin hormone stimulates glyconeogenesis, lipolysis and anabolism in maternal organs, and influences fetal growth, placental development and maternal adaptation to pregnancy...
August 2017: Biomedical Reports
https://www.readbyqxmd.com/read/28801532/activation-of-nkx2-5-calr-p53-signaling-pathway-by-hyperglycemia-induces-cardiac-remodeling-and-dysfunction-in-adult-zebrafish
#15
Sun Yanyi, Wang Qiuyun, Fang Yuehua, Wu Chunfang, Lu Guoping, Chen Zhenyue
Hyperglycemia is an independent risk factor for diabetic cardiomyopathy in humans; however, the underlying mechanisms have not been thoroughly elucidated. Zebrafish (Danio rerio) was used in this study as a novel vertebrate model to explore the signaling pathways of human adult cardiomyopathy. Hyperglycemia was induced by alternately immersing adult zebrafish in a glucose solution or water. The hyperglycemic fish gradually exhibited some hallmarks of cardiomyopathy such as myocardial hypertrophy and apoptosis, myofibril loss, fetal gene reactivation, and severe arrhythmia...
August 11, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28799096/a-quantitative-and-qualitative-rna-expression-profiling-assay-for-cell-culture-with-single-cell-resolution
#16
Petra Kraus, Rachel Yerden, Darren Sipes, Shantanu Sur, Thomas Lufkin
Cells are often characterized by their gene expression profile. However, commonly used methods to detect mRNA require cell pooling and could therefore mask differences in gene expression within heterogeneous cell populations. q(2)PISH allows for the analysis of both qualitative and quantitative (q(2)) gene expression on cultured cells for quality control measures with single cell resolution. q(2)PISH was optimized for the subsequent use of two alkaline phosphatase substrates in combination with a cell nucleus count to allow for accurate quantification of gene expression per cell and simultaneously qualitative assessment of potential culture population drift or heterogeneity...
August 10, 2017: Cytotechnology
https://www.readbyqxmd.com/read/28798665/maternal-diabetes-alters-expression-of-micrornas-that-regulate-genes-critical-for-neural-tube-development
#17
Seshadri Ramya, Sukanya Shyamasundar, Boon Huat Bay, S Thameem Dheen
Maternal diabetes is known to cause neural tube defects (NTDs) in embryos and neuropsychological deficits in infants. Several metabolic pathways and a plethora of genes have been identified to be deregulated in developing brain of embryos by maternal diabetes, although the exact mechanism remains unknown. Recently, miRNAs have been shown to regulate genes involved in brain development and maturation. Therefore, we hypothesized that maternal diabetes alters the expression of miRNAs that regulate genes involved in biological pathways critical for neural tube development and closure during embryogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28796236/genetic-disruption-of-the-oncogenic-hmga2-plag1-igf2-pathway-causes-fetal-growth-restriction
#18
Walid Abi Habib, Frédéric Brioude, Thomas Edouard, James T Bennett, Anne Lienhardt-Roussie, Frédérique Tixier, Jennifer Salem, Tony Yuen, Salah Azzi, Yves Le Bouc, Madeleine D Harbison, Irène Netchine
PurposeFetal growth is a complex process involving maternal, placental and fetal factors. The etiology of fetal growth retardation remains unknown in many cases. The aim of this study is to identify novel human mutations and genes related to Silver-Russell syndrome (SRS), a syndromic form of fetal growth retardation, usually caused by epigenetic downregulation of the potent fetal growth factor IGF2.MethodsWhole-exome sequencing was carried out on members of an SRS familial case. The candidate gene from the familial case and two other genes were screened by targeted high-throughput sequencing in a large cohort of suspected SRS patients...
August 10, 2017: Genetics in Medicine: Official Journal of the American College of Medical Genetics
https://www.readbyqxmd.com/read/28794470/endocrine-disruptors-induce-perturbations-in-endoplasmic-reticulum-and-mitochondria-of-human-pluripotent-stem-cell-derivatives
#19
Uthra Rajamani, Andrew R Gross, Camille Ocampo, Allen M Andres, Roberta A Gottlieb, Dhruv Sareen
Persistent exposure to man-made endocrine disrupting chemicals during fetal endocrine development may lead to disruption of metabolic homeostasis contributing to childhood obesity. Limited cellular platforms exist to test endocrine disrupting chemical-induced developmental abnormalities in human endocrine tissues. Here we use an human-induced pluripotent stem cell-based platform to demonstrate adverse impacts of obesogenic endocrine disrupting chemicals in the developing endocrine system. We delineate the effects upon physiological low-dose exposure to ubiquitous endocrine disrupting chemicals including, perfluoro-octanoic acid, tributyltin, and butylhydroxytoluene, in endocrine-active human-induced pluripotent stem cell-derived foregut epithelial cells and hypothalamic neurons...
August 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28793237/fetal-sex-dependent-genomic-responses-in-the-circulating-lymphocytes-of-arsenic-exposed-pregnant-women-in-new-hampshire
#20
Paige A Bommarito, Elizabeth Martin, Lisa Smeester, Thomas Palys, Emily R Baker, Margaret R Karagas, Rebecca C Fry
Exposure to inorganic arsenic (iAs) during pregnancy is associated with adverse health outcomes present both at birth and later in life. A mechanism may include epigenetic and genomic alteration in fetal genes involved in immune functioning. To investigate the role of the maternal immune response to in utero iAs exposure, we conducted an analysis of immune-related genes in pregnant women from the New Hampshire Birth Cohort Study. A set of 31 genes were identified with altered expression in association with levels of urinary total arsenic, urinary iAs, urinary monomethylated arsenic and urinary dimethylated arsenic...
August 6, 2017: Reproductive Toxicology
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