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DOI 10.1002/bdrb.21063

Медицинская библиотека · Birth defects research. Part B, Developmental and reproductive toxicology · 2013

Ethanol alters proliferation and differentiation of normal and chromosomally abnormal human embryonic stem cell-derived neurospheres.

Krishnamoorthy Malini, Gerwe Brian A, Scharer Christopher D, Sahasranaman Vanita, Eilertson Carmen D, Nash Rachel J, Usta Sümeyra Naz, Kelly Shasmine, Rose Matthew, Peraza Rene, Arumugham Jagan, Stewart Bethany, Stice Steven L, Nash Rodney J

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Аннотация

Ethanol is a powerful substance and, when consumed during pregnancy, has significant psychoactive and developmental effects on the developing fetus. These abnormalities include growth retardation, neurological deficits, and behavioral and cognitive deficiencies, commonly referred to as fetal alcohol spectrum disorder. The effect of ethanol has been reported to affect cellular development on the embryonic level, however, not much is known about mutations contributing to the influence of ethanol. The purpose of our study was to determine if mutation contribute to changes in differentiation patterning, cell-cycle regulatory gene expression, and DNA methylation in human embryonic stem cells after ethanol exposure. We exposed human embryonic stem cells (with and without know DNA mutations) to a low concentration (20 mM) of ethanol and measured neurosphere proliferation and differentiation, glial protein levels, expression of various cell-cycle genes, and DNA methylation. Ethanol altered cell-cycle gene expression between the two cell lines; however, gene methylation was not affected in ether lines.

Для цитирования: Krishnamoorthy Malini, Gerwe Brian A, Scharer Christopher D, Sahasranaman Vanita, Eilertson Carmen D, Nash Rachel J, Usta Sümeyra Naz, Kelly Shasmine, Rose Matthew, Peraza Rene, Arumugham Jagan, Stewart Bethany, Stice Steven L, Nash Rodney J. Ethanol alters proliferation and differentiation of normal and chromosomally abnormal human embryonic stem cell-derived neurospheres.. Birth defects research. Part B, Developmental and reproductive toxicology. 2013. DOI: 10.1002/bdrb.21063.

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