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Theresa L. Powell

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https://www.readbyqxmd.com/read/28814482/lrig1-gastric-isthmal-progenitor-cells-restore-normal-gastric-lineage-cells-during-damage-recovery-in-adult-mouse-stomach
#1
Eunyoung Choi, Tyler L Lantz, Gregory Vlacich, Theresa M Keeley, Linda C Samuelson, Robert J Coffey, James R Goldenring, Anne E Powell
OBJECTIVE: Lrig1 is a marker of proliferative and quiescent stem cells in the skin and intestine. We examined whether Lrig1-expressing cells are long-lived gastric progenitors in gastric glands in the mouse stomach. We also investigated how the Lrig1-expressing progenitor cells contribute to the regeneration of normal gastric mucosa by lineage commitment to parietal cells after acute gastric injury in mice. DESIGN: We performed lineage labelling using Lrig1-CreERT2/+;R26R-YFP/+ (Lrig1/YFP) or R26R-LacZ/+ (Lrig1/LacZ) mice to examine whether the Lrig1-YFP-marked cells are gastric progenitor cells...
August 16, 2017: Gut
https://www.readbyqxmd.com/read/28651693/fatty-acid-and-lipid-profiles-in-primary-human-trophoblast-over-90h-in-culture
#2
Véronique Ferchaud-Roucher, Michael C Rudolph, Thomas Jansson, Theresa L Powell
Little is known about the mechanisms underlying the preferential transport of long chain polyunsaturated fatty acids (LCPUFA) to the fetus by the syncytiotrophoblast and the role of cytotrophoblasts in placental lipid metabolism and transport. We studied primary human trophoblast (PHT) cells cultured for 90h to determine the fatty acid and lipid composition of cytotrophoblast (18h culture) and syncytiotrophoblast (90h culture) cells. In cultured PHT total lipid fatty acids were significantly (P < 0.05) reduced at 90h compared to 18h in culture including lower levels of palmitic acid (PA, 16:0, -37%), palmitoleic acid (POA, 16:1n-7, -30%), oleic acid (OA, 18:1n-9, -31%), LCPUFA arachidonic acid (AA, 20:4n-6, -28%) and α-linolenic acid (ALA, 18:3n-3, -55%)...
June 2017: Prostaglandins, Leukotrienes, and Essential Fatty Acids
https://www.readbyqxmd.com/read/28638048/maternal-folate-deficiency-causes-inhibition-of-mtor-signaling-down-regulation-of-placental-amino-acid-transporters-and-fetal-growth-restriction-in-mice
#3
Fredrick J Rosario, Peter W Nathanielsz, Theresa L Powell, Thomas Jansson
Maternal folate deficiency is linked to restricted fetal growth, however the underlying mechanisms remain to be established. Here we tested the hypothesis that mTOR functions as a folate sensor in vivo in mice and that maternal folate deficiency inhibits placental mTOR signaling and amino acid transporter activity and causes fetal growth restriction. Folate deficient mice had lower serum folate (-60%). In late pregnancy, fetal weight in the folate deficient group was decreased (-17%, p < 0.05), whereas placental weight, litter size and crown rump length were unaltered...
June 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28592519/mechanistic-target-of-rapamycin-is-a-novel-molecular-mechanism-linking-folate-availability-and-cell-function
#4
REVIEW
Elena Silva, Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Folate deficiency has been linked to a wide range of disorders, including cancer, neural tube defects, and fetal growth restriction. Folate regulates cellular function mediated by its involvement in the synthesis of nucleotides, which are needed for DNA synthesis, and its function as a methyl donor, which is critical for DNA methylation. Here we review current data showing that folate sensing by mechanistic target of rapamycin (mTOR) constitutes a novel and distinct pathway by which folate modulates cell functions such as nutrient transport, protein synthesis, and mitochondrial respiration...
July 2017: Journal of Nutrition
https://www.readbyqxmd.com/read/28574453/randomized-controlled-trial-of-dha-supplementation-during-pregnancy-child-adiposity-outcomes
#5
Byron A Foster, Elia Escaname, Theresa L Powell, Benjamin Larsen, Sartaj K Siddiqui, John Menchaca, Christian Aquino, Rajam Ramamurthy, Daniel E Hale
Investigating safe and effective interventions in pregnancy that lower offspring adiposity is important given the burden of obesity and subsequent metabolic derangements. Our objective was to determine if docosahexaenoic acid (DHA) given during pregnancy to obese mothers results in lower offspring adiposity. This study was a long-term follow-up of a randomized trial of mothers with gestational diabetes or obesity who were randomized to receive DHA supplementation at 800 mg/day or placebo (corn/soy oil) starting at 25-29 weeks gestation...
June 2, 2017: Nutrients
https://www.readbyqxmd.com/read/28374905/mtor-folate-sensing-links-folate-availability-to-trophoblast-cell-function
#6
Fredrick J Rosario, Theresa L Powell, Thomas Jansson
KEY POINTS: Folate deficiency during pregnancy is associated with restricted fetal growth, although the underlying mechanisms are poorly understood. Here we show that mechanistic target of rapamycin (mTOR) functions as a folate sensor in primary human trophoblast (PHT) cells. Folate sensing by mTOR in PHT cells involves both mTOR Complex 1 and 2 and requires the proton-coupled folate transporter. We report a previously unknown molecular mechanism by which folate regulates trophoblast cell function...
July 1, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/27956114/1-25-dihydroxy-vitamin-d3-stimulates-system-a-amino-acid-transport-in-primary-human-trophoblast-cells
#7
Yi-Yung Chen, Theresa L Powell, Thomas Jansson
Vitamin D deficiency during pregnancy is linked to adverse perinatal outcomes such as small for gestational age infants. Recent evidence suggests that changes in placental amino acid transport contribute to altered fetal growth. We tested the hypothesis that 1,25-dihydroxy vitamin D3 increases the gene expression of System A and L amino acid transporter isoforms and stimulates placental amino acid transport activity in cultured primary human trophoblast cells mediated by mTOR signaling. Treatment with 1,25-dihydroxy vitamin D3 significantly increased mRNA expression of the System A isoform SNAT2 and System A activity, but had no effect on System L and did not affect mTOR signaling...
February 15, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27776119/fetus-derived-dlk1-is-required-for-maternal-metabolic-adaptations-to-pregnancy-and-is-associated-with-fetal-growth-restriction
#8
Mary A M Cleaton, Claire L Dent, Mark Howard, Jennifer A Corish, Isabelle Gutteridge, Ulla Sovio, Francesca Gaccioli, Nozomi Takahashi, Steven R Bauer, D Steven Charnock-Jones, Theresa L Powell, Gordon C S Smith, Anne C Ferguson-Smith, Marika Charalambous
Pregnancy is a state of high metabolic demand. Fasting diverts metabolism to fatty acid oxidation, and the fasted response occurs much more rapidly in pregnant women than in non-pregnant women. The product of the imprinted DLK1 gene (delta-like homolog 1) is an endocrine signaling molecule that reaches a high concentration in the maternal circulation during late pregnancy. By using mouse models with deleted Dlk1, we show that the fetus is the source of maternal circulating DLK1. In the absence of fetally derived DLK1, the maternal fasting response is impaired...
December 2016: Nature Genetics
https://www.readbyqxmd.com/read/27605346/down-regulation-of-placental-transport-of-amino-acids-precedes-the-development-of-intrauterine-growth-restriction-in-maternal-nutrient-restricted-baboons
#9
Priyadarshini Pantham, Fredrick J Rosario, Susan T Weintraub, Peter W Nathanielsz, Theresa L Powell, Cun Li, Thomas Jansson
Intrauterine growth restriction (IUGR) is an important risk factor for perinatal complications and adult disease. IUGR is associated with down-regulation of placental amino acid transporter expression and activity at birth. It is unknown whether these changes are a cause or a consequence of human IUGR. We hypothesized that placental amino acid transport capacity is reduced prior to onset of reduced fetal growth in baboons with maternal nutrient restriction (MNR). Pregnant baboons were fed either a control (n = 8) or MNR diet (70% of control diet, n = 9) from Gestational Day 30...
November 2016: Biology of Reproduction
https://www.readbyqxmd.com/read/27587625/ovarian-cancer-version-1-2016-nccn-clinical-practice-guidelines-in-oncology
#10
Robert J Morgan, Deborah K Armstrong, Ronald D Alvarez, Jamie N Bakkum-Gamez, Kian Behbakht, Lee-May Chen, Larry Copeland, Marta Ann Crispens, Maria DeRosa, Oliver Dorigo, David M Gershenson, Heidi J Gray, Ardeshir Hakam, Laura J Havrilesky, Carolyn Johnston, Shashikant Lele, Lainie Martin, Ursula A Matulonis, David M O'Malley, Richard T Penson, Sanja Percac-Lima, Mario Pineda, Steven C Plaxe, Matthew A Powell, Elena Ratner, Steven W Remmenga, Peter G Rose, Paul Sabbatini, Joseph T Santoso, Theresa L Werner, Jennifer Burns, Miranda Hughes
This selection from the NCCN Guidelines for Ovarian Cancer focuses on the less common ovarian histopathologies (LCOHs), because new algorithms were added for LCOHs and current algorithms were revised for the 2016 update. The new LCOHs algorithms include clear cell carcinomas, mucinous carcinomas, and grade 1 (low-grade) serous carcinomas/endometrioid epithelial carcinomas. The LCOHs also include carcinosarcomas (malignant mixed Müllerian tumors of the ovary), borderline epithelial tumors (also known as low malignant potential tumors), malignant sex cord-stromal tumors, and malignant germ cell tumors...
September 2016: Journal of the National Comprehensive Cancer Network: JNCCN
https://www.readbyqxmd.com/read/27562465/mechanistic-target-of-rapamycin-mtor-regulates-trophoblast-folate-uptake-by-modulating-the-cell-surface-expression-of-fr-%C3%AE-and-the-rfc
#11
Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Folate deficiency in fetal life is strongly associated with structural malformations and linked to intrauterine growth restriction. In addition, limited availability of methyl donors, such as folate, during pregnancy may result in abnormal gene methylation patterns and contribute to developmental programming. The fetus is dependent on placental transfer of folate, however the molecular mechanisms regulating placental folate transport are unknown. We used cultured primary human trophoblast cells to test the hypothesis that mechanistic target of rapamycin complex 1 (mTORC1) and 2 (mTORC2) regulate folate transport by post-translational mechanisms...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27038902/perfluorinated-alkyl-acids-in-the-plasma-of-south-african-crocodiles-crocodylus-niloticus
#12
Ian Christie, Jessica L Reiner, John A Bowden, Hannes Botha, Theresa M Cantu, Danny Govender, Matthew P Guillette, Russell H Lowers, Wilmien J Luus-Powell, Danie Pienaar, Willem J Smit, Louis J Guillette
Perfluorinated alkyl acids (PFAAs) are environmental contaminants that have been used in many products for over 50 years. Interest and concern has grown since 2000 on the widespread presence of PFAAs, when it was discovered that PFAAs were present in wildlife samples around the northern hemisphere. Since then, several studies have reported PFAAs in wildlife from many locations, including the remote regions of Antarctica and the Arctic. Although there are a multitude of studies, few have reported PFAA concentrations in reptiles and wildlife in the Southern Hemisphere...
July 2016: Chemosphere
https://www.readbyqxmd.com/read/27016784/protein-expression-of-fatty-acid-transporter-2-is-polarized-to-the-trophoblast-basal-plasma-membrane-and-increased-in-placentas-from-overweight-obese-women
#13
COMPARATIVE STUDY
Susanne Lager, Vanessa I Ramirez, Francesca Gaccioli, Brian Jang, Thomas Jansson, Theresa L Powell
BACKGROUND: Obese and overweight women are more likely to deliver a large infant or an infant with increased adiposity, however the underlying mechanisms are not well established. We tested the hypothesis that placental capacity to transport fatty acid is increased in overweight/obese women. METHODS: Pregnant women with body mass index (BMI) ranging from 18.4 to 54.3 kg/m(2) and with uncomplicated term pregnancies were recruited for collection of blood samples and placental tissue...
April 2016: Placenta
https://www.readbyqxmd.com/read/26858656/placental-responses-to-changes-in-the-maternal-environment-determine-fetal-growth
#14
REVIEW
Kris Genelyn Dimasuay, Philippe Boeuf, Theresa L Powell, Thomas Jansson
Placental responses to maternal perturbations are complex and remain poorly understood. Altered maternal environment during pregnancy such as hypoxia, stress, obesity, diabetes, toxins, altered nutrition, inflammation, and reduced utero-placental blood flow may influence fetal development, which can predispose to diseases later in life. The placenta being a metabolically active tissue responds to these perturbations by regulating the fetal supply of nutrients and oxygen and secretion of hormones into the maternal and fetal circulation...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/26747729/a-novel-rat-model-of-gestational-diabetes-induced-by-intrauterine-programming-is-associated-with-alterations-in-placental-signaling-and-fetal-overgrowth
#15
Evangelina Capobianco, Daiana Fornes, Ivana Linenberg, Theresa L Powell, Thomas Jansson, Alicia Jawerbaum
A family history of diabetes predisposes to gestational diabetes mellitus (GDM). We hypothesized that female offspring of rats with pre-gestational diabetes will develop GDM, a pathology associated with fetal overgrowth and altered placental signaling. We found normal glycemia and insulinemia in the offspring from pre-gestational diabetic rats at three months of age. However, consistent with GDM, maternal hyperglycemia and hyperinsulinemia and increased fetal weight were evident when compared to controls. In this intrauterine programmed GDM model, the placentas showed alterations in mTOR pathway: unchanged phosphorylation of 4EBP-1 and PKCα despite reduced total expression of 4EBP-1 and PKCα, and increased phosphorylation of SGK1...
February 15, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/26608079/regulation-of-amino-acid-transporter-trafficking-by-mtorc1-in-primary-human-trophoblast-cells-is-mediated-by-the-ubiquitin-ligase-nedd4-2
#16
Fredrick J Rosario, Kris Genelyn Dimasuay, Yoshikatsu Kanai, Theresa L Powell, Thomas Jansson
Changes in placental amino acid transfer directly contribute to altered fetal growth, which increases the risk for perinatal complications and predisposes for the development of obesity, diabetes and cardiovascular disease later in life. Placental amino acid transfer is critically dependent on the expression of specific transporters in the plasma membrane of the trophoblast, the transporting epithelium of the human placenta. However, the molecular mechanisms regulating this process are largely unknown. Nedd4-2 is an ubiquitin ligase that catalyses the ubiquitination of proteins, resulting in proteasomal degradation...
April 1, 2016: Clinical Science (1979-)
https://www.readbyqxmd.com/read/26508738/tnf-%C3%AE-stimulates-system-a-amino-acid-transport-in-primary-human-trophoblast-cells-mediated-by-p38-mapk-signaling
#17
Irving L M H Aye, Thomas Jansson, Theresa L Powell
Maternal obesity and gestational diabetes mellitus (GDM) increase the risk of delivering infants that are large for gestational age with greater adiposity, who are prone to the development of metabolic disease in childhood and beyond. These maternal conditions are also associated with increased levels of the proinflammatory cytokine TNF-α in maternal tissues and the placenta. Recent evidence suggests that changes in placental amino acid transport contribute to altered fetal growth. TNF-α was previously shown to stimulate System A amino acid transport in primary human trophoblasts (PHTs), however the molecular mechanisms remain unknown...
October 2015: Physiological Reports
https://www.readbyqxmd.com/read/26491104/increased-placental-fatty-acid-transporter-6-and-binding-protein-3-expression-and-fetal-liver-lipid-accumulation-in-a-mouse-model-of-obesity-in-pregnancy
#18
Paula Díaz, Jessica Harris, Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Obesity in pregnancy is associated with increased fetal growth and adiposity, which, in part, is determined by transplacental nutrient supply. Trophoblast uptake and intracellular trafficking of lipids are dependent on placental fatty acid transport proteins (FATP), translocase (FAT/CD36), and fatty acid binding proteins (FABP). We hypothesized that maternal obesity in mice leads to increased placental expression of FAT/CD36, FATPs, and FABPs, and lipid accumulation in the fetal liver. C57/BL6J female mice were fed either a control (C; n = 10) or an obesogenic (OB; n = 10) high-fat, high-sugar diet before mating and throughout pregnancy...
December 15, 2015: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/26491103/activation-of-placental-insulin-and-mtor-signaling-in-a-mouse-model-of-maternal-obesity-associated-with-fetal-overgrowth
#19
Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Fetal overgrowth is common in obese women and is associated with perinatal complications and increased risk for the child to develop metabolic syndrome later in life. Placental nutrient transport capacity has been reported to be increased in obese women giving birth to large infants; however, the underlying mechanisms are not well established. Obesity in pregnancy is characterized by elevated maternal serum insulin and leptin, hormones that stimulate placental amino acid transporters in vitro. We hypothesized that maternal obesity activates placental insulin/IGF-I/mTOR and leptin signaling pathways...
January 1, 2016: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/26417088/adiponectin-supplementation-in-pregnant-mice-prevents-the-adverse-effects-of-maternal-obesity-on-placental-function-and-fetal-growth
#20
Irving L M H Aye, Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth...
October 13, 2015: Proceedings of the National Academy of Sciences of the United States of America
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