Dioxin exposure disrupts the differentiation of mouse embryonic stem cells into cardiomyocytes.

ABSTRACT: Experimental exposure of fish, birds, and rodents to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) causes multiple Ah receptor-mediated developmental abnormalities, an observation consistent with compelling evidence in human populations that TCDD exposure is responsible for a significant incidence of birth defects. To characterize molecular mechanisms that might explain the developmental effects of dioxin, we have studied the consequences of TCDD exposure on the differentiation of mouse embryonic stem (ES) cells in culture and on the expression of genes, including those coding for homeodomain containing transcription factors, with a role in progression of tissue differentiation and embryonic identity during development. We find that TCDD treatment causes expression changes in a number

SUBMITTER: Wang Y 

PROVIDER: S-EPMC2855359 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature