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Your search keyword '"Hyde, Emily"' showing total 3 results
Start Over Author "Hyde, Emily" Topic metabolism
3 results on '"Hyde, Emily"'

1. Use of metagenomics and metatranscriptomics to determine the influence of organic sulfur compounds on the sulfur cycle in the sediment of a low-sulfate freshwater system

Author

Hyde, Emily

Subjects
Freshwater, Metabolism, Metagenomics, Metatranscriptomics, Organic, Sulfur
Abstract

The sulfur cycle is an important and complex biogeochemical cycle involving both inorganic and organic species in both oxic and anoxic environments. However, due to the lack of research regarding the sulfur cycle in freshwater systems, the contributions of organic sulfur compounds to the sulfur cycle are underappreciated. Recent studies have suggested organic sulfur compounds likely fuels sulfate reduction, especially in low-sulfate oligotrophic freshwater systems, through a possible cryptic sulfur cycle. To determine the contributions that organic sulfur compounds may have in this environment, we used Lake Superior sediment to analyze for the presence of and expression of sulfur cycling genes. In these metagenomes, we found genes for sulfur reduction, oxidation and organic sulfur compound degradation. Metabolic pathway analysis showed presence of not only organic sulfur compounds contributing to the sulfur cycle, but tetrathionate, thiosulfate, and polysulfides playing a role as well. Using Lake Superior sediments, we also conducted sediment incubations to measure the biotransformation capability of sulfur-containing amino acids, sulfonates, and an analog for a common sulfolipid. Taurine and sodium dodecyl sulfate produced higher sulfate values in incubations, suggesting that microbes prefer sulfonates over sulfur-containing amino acids, in addition to a possible partiality towards oxidized organic sulfur compounds over reduced forms regarding sulfate production. The preference of sulfonates is supported by the commonality of taurine genes present as well as the low, but present transcription values of sulfoacetaldehyde degradation. While sulfur-containing amino acids do not produce sulfate values near that of sulfonates or sulfolipids, there are still present and transcriptionally active genes that can contribute to sulfate reduction in the system. Regarding methyl-sulfurs, metatranscriptomic data shows that methyl-mercaptan (intermediate within dimethyl sulfide and methionine degradation) degradation is transcriptionally active across genomes. By combining biotransformation incubation data, metagenomics, and metatranscriptomics, we analyzed how methylated sulfurs, sulfur-containing amino acids and sulfonates can fuel a sulfur cycle in a low-sulfate environment, informing us on how pathways may have operated in our Earth’s geologic past.

Published
2020

2. Placental uptake and metabolism of 25(OH)vitamin D determine its activity within the fetoplacental unit.

Author

Ashley, Brogan, Simner, Claire, Manousopoulou, Antigoni, Jenkinson, Carl, Hey, Felicity, Frost, Jennifer M., Rezwan, Faisal I., White, Cory H., Lofthouse, Emma M., Hyde, Emily, Cooke, Laura D. F., Barton, Sheila, Mahon, Pamela, Curtis, Elizabeth M., Moon, Rebecca J., Crozier, Sarah R., Inskip, Hazel M., Godfrey, Keith M., Holloway, John W., and Cooper, Cyrus

Subjects
*FETAL physiology, *VITAMIN D metabolism, *PLACENTA, *VITAMIN D, *METABOLISM, *VITAMINS, *CALCIUM metabolism
Abstract

Pregnancy 25-hydroxyvitamin D [25(OH)D] concentrations are associated with maternal and fetal health outcomes. Using physiological human placental perfusion and villous explants, we investigate the role of the placenta in regulating the relationships between maternal 25(OH)D and fetal physiology. We demonstrate active placental uptake of 25(OH)D3 by endocytosis, placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the maternal and fetal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than simply the availability of maternal 25(OH) D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta, with widespread effects on the placenta itself. These data demonstrate a complex interplay between vitamin D and the placenta and will inform future interventions using vitamin D to support fetal development and maternal adaptations to pregnancy. [ABSTRACT FROM AUTHOR]

Published
2022
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3. Placental uptake and metabolism of 25(OH)vitamin D determine its activity within the fetoplacental unit

Author

Emily Hyde, Sheila J. Barton, Miguel R. Branco, Cory H. White, Spiros D Garbis, Claire Simner, Faisal I. Rezwan, Nicholas C. Harvey, P A Mahon, Rebecca J Moon, Felicity Hey, Kerry S Jones, Martin Hewison, Cyrus Cooper, John W. Holloway, Antigoni Manousopoulou, Elizabeth M Curtis, Carl Jenkinson, Hazel Inskip, Sarah Crozier, Rohan M. Lewis, Brogan Ashley, Emma M. Lofthouse, Laura Cooke, Jennifer M. Frost, Jane K. Cleal, Keith M. Godfrey, Jones, Kerry [0000-0002-7380-9797], Apollo - University of Cambridge Repository, Jenkinson, Carl [0000-0002-1838-5282], Hey, Felicity [0000-0003-2695-4817], Frost, Jennifer M [0000-0002-3057-6313], Rezwan, Faisal I [0000-0001-9921-222X], White, Cory H [0000-0002-1619-0174], Lofthouse, Emma M [0000-0002-0175-5590], Hyde, Emily [0000-0001-5084-3709], Cooke, Laura DF [0000-0002-8099-9437], Barton, Sheila [0000-0003-4963-4242], Mahon, Pamela [0000-0003-0661-572X], Curtis, Elizabeth M [0000-0002-5147-0550], Moon, Rebecca J [0000-0003-2334-2284], Crozier, Sarah R [0000-0002-9524-1127], Inskip, Hazel M [0000-0001-8897-1749], Godfrey, Keith M [0000-0002-4643-0618], Holloway, John W [0000-0001-9998-0464], Cooper, Cyrus [0000-0003-3510-0709], Lewis, Rohan M [0000-0003-4044-9104], Hewison, Martin [0000-0001-5806-9690], Garbis, Spiros DD [0000-0002-1050-0805], Branco, Miguel R [0000-0001-9447-1548], Harvey, Nicholas C [0000-0002-8194-2512], and Cleal, Jane K [0000-0001-7978-4327]

Subjects
medicine.medical_specialty, placenta, 030209 endocrinology & metabolism, Endocytosis, General Biochemistry, Genetics and Molecular Biology, Transcriptome, 03 medical and health sciences, transcriptomics, 0302 clinical medicine, Fetus, Pregnancy, Placenta, Internal medicine, medicine, Vitamin D and neurology, Humans, Epigenetics, Vitamin D, 030304 developmental biology, Calcifediol, 0303 health sciences, General Immunology and Microbiology, epigenetics, Chemistry, General Neuroscience, General Medicine, Metabolism, Vitamins, medicine.disease, 3. Good health, Endocrinology, medicine.anatomical_structure, fetal programming, embryonic structures, Female, General Economics, Econometrics and Finance, Research Article, Developmental Biology, Human
Abstract

Funder: Gerald Kerkut Charitable Trust; FundRef: http://dx.doi.org/10.13039/100012166, Funder: Rank Prize, Funder: NIHR Clinical Lectureship, Pregnancy 25-hydroxyvitamin D [25(OH)D] concentrations are associated with maternal and fetal health outcomes. Using physiological human placental perfusion and villous explants, we investigate the role of the placenta in regulating the relationships between maternal 25(OH)D and fetal physiology. We demonstrate active placental uptake of 25(OH)D3 by endocytosis, placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the maternal and fetal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than simply the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta, with widespread effects on the placenta itself. These data demonstrate a complex interplay between vitamin D and the placenta and will inform future interventions using vitamin D to support fetal development and maternal adaptations to pregnancy., CS was funded by a Gerald Kerkut Charitable Trust studentship and BA by Rank Prize and University of Southampton Vice Chancellor���s Studentships plus the MRC. KMG was supported by the UK Medical Research Council (MC_UU_12011/4), the National Institute for Health Research (NIHR Senior Investigator [NF-SI-0515-10042], NIHR Southampton 1000DaysPlus Global Nutrition Research Group [17/63/154], and NIHR Southampton Biomedical Research Centre [IS-BRC-1215-20004]), British Heart Foundation (RG/15/17/3174) and the US National Institute on Aging of the National Institutes of Health (Award No. U24AG047867). KSJ was supported by the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (ISBRC-1215-20014). The NIHR Cambridge Biomedical Research Centre is a partnership between Cambridge University Hospitals NHS Foundation Trust and the University of Cambridge, funded by the NIHR. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care. Experimental work performed by KSJ and FH at MRC. EWL was supported by Dr Ann Prentice (UK Medical Research Council U105960371). The SWS has been supported by grants from Medical Research Council (MRC) (4050502589 [MRC LEU]), Dunhill Medical Trust, British Heart Foundation, Food Standards Agency, National Institute for Health Research (NIHR) Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, NIHR Oxford Biomedical Research Centre, University of Oxford, and the European Union���s Seventh Framework Programme (FP7/2007-2013), project EarlyNutrition, under grant agreement 289346 and the European Union���s Horizon 2020 research and innovation program (LIFECYCLE, grant agreement no. 733206). EC has been supported by the Wellcome Trust (201268/Z/16/Z) and an NIHR Clinical Lectureship. Work leading to these results was supported by the BBSRC (HDHL-Biomarkers, BB/P028179/1), as part of the ALPHABET project, supported by an award made through the ERA-Net on Biomarkers for Nutrition and Health (ERA HDHL), Horizon 2020 grant agreement number 696295. The proteomic analyses (SDG and AM) were financially supported by the National Institutes of Health (R21AI122389) and the Beckman Institute at the California Institute of Technology. This project has received funding from the European Union���s Horizon 2020 research and innovation program under the Marie Sk��odowska-Curie grant agreement InvADeRS no. 841172 to JMF. The electron microscopy image in Figure 2 was produced with help of the Biomedical imaging unit, Faculty of Medicine, University of Southampton.

Published
2022
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