Works (4)
Updated: June 19th, 2023 22:06
2022 article
Epigenetic control of the imprinted growth regulator Cdkn1c in cadmium-induced placental dysfunction
Simmers, M. D., Hudson, K. M., Baptissart, M., & Cowley, M. (2022, July 1). EPIGENETICS, Vol. 7.
author keywords: Genomic imprinting; imprinted genes; DNA methylation; placenta; cadmium; foetal growth restriction; CDKN1C; toxic metal
TL;DR:
It is concluded that the Cd-associated increase in Cdkn1c expression can be fully explained by alterations to placental structure, and it is shown that CdKn1c is expressed primarily in the placental labyrinth which is proportionally increased in size in response to Cd.
(via Semantic Scholar)
open access via www.tandfonline.com (publisher PDF)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, ORCID, NC State University Libraries
Added: July 11, 2022
2022 article
The imprinted gene Zac1 regulates steatosis in developmental cadmium-induced nonalcoholic fatty liver disease
Riegl, S. D., Starnes, C., Jima, D. D., Baptissart, M., Diehl, A. M., Belcher, S. M., & Cowley, M. (2022, October 6). TOXICOLOGICAL SCIENCES, Vol. 10.
author keywords: nonalcoholic fatty liver disease; developmental toxicology; epigenetics; cadmium; genomic imprinting; developmental programming
MeSH headings : Mice; Animals; Non-alcoholic Fatty Liver Disease / genetics; Non-alcoholic Fatty Liver Disease / metabolism; Cadmium; Cadmium Chloride / toxicity; PPAR gamma; Liver / metabolism; Fibrosis
TL;DR:
It is demonstrated that developmental Cd exposure is sufficient to program NAFLD in later life, and Zac1 and the IGN are established as key regulators of prosteatotic and profibrotic pathways, two of the major pathological hallmarks ofNAFLD.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, ORCID, NC State University Libraries
Added: October 29, 2022
2022 article
Zac1 and the Imprinted Gene Network program juvenile NAFLD in response to maternal metabolic syndrome
Baptissart, M., Bradish, C. M., Jones, B. S., Walsh, E., Tehrani, J., Marrero-Colon, V., … Cowley, M. (2022, February 28). HEPATOLOGY, Vol. 2.
MeSH headings : Animals; Cell Cycle Proteins / genetics; Cell Cycle Proteins / metabolism; Disease Models, Animal; Gene Regulatory Networks / genetics; Gene Regulatory Networks / physiology; Genes, Tumor Suppressor / physiology; Metabolic Syndrome / complications; Metabolic Syndrome / genetics; Metabolic Syndrome / metabolism; Mice; Non-alcoholic Fatty Liver Disease / complications; Non-alcoholic Fatty Liver Disease / genetics; Non-alcoholic Fatty Liver Disease / metabolism; Transcription Factors / genetics; Transcription Factors / metabolism; Transforming Growth Factor beta1
TL;DR:
It is hypothesized that imprinted genes, defined by expression from a single parental allele, play a key role in maternal MetS‐induced NAFLD, due to their susceptibility to environmental stressors and their functions in liver homeostasis.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: March 28, 2022
2018 journal article
Neonatal mice exposed to a high-fat diet in utero influence the behaviour of their nursing dam
Proceedings of the Royal Society B: Biological Sciences, 285(1891), 20181237.
Contributors: n, H. Lamb n, K. To n, C. Bradish n , J. Tehrani n, D. Reif n , M. Cowley n
MeSH headings : Animals; Animals, Newborn / physiology; Diet, High-Fat; Female; Maternal Behavior / physiology; Maternal Exposure; Mice / physiology; Mice, Inbred C57BL; Pregnancy
TL;DR:
In utero exposure to HF diet programmes physiological changes in the offspring which influence the maternal behaviours of their dam after birth are suggested.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: NC State University Libraries, ORCID, NC State University Libraries
Added: December 10, 2018
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