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Bisphenol A enhances retinoic acid-HOX genes signaling disrupting brain development: human

ABSTRACT: Plastic pollution and exposure to endocrine- disrupting chemicals (EDCs) like Bisphenol A (BPA) are emerging environmental concerns with potential impacts on human health and development. Despite evidence from epidemiological studies linking chemical exposure1,2 to neurodevelopmental disorders such as autism spectrum disorder and attention deficit hyperactivity disorder, the underlying causal mechanisms remain unclear3. Here, we show quantitative evidence that chemical exposure and detrimental outcomes are mechanistically linked to interference with retinoic acid (RA) signaling, a critical pathway in brain and neuronal development. Utilizing human induced pluripotent stem cells and zebrafish embryos, we found that BPA potentiated exogenous RA effects on 3′HOX gene expression and brain patterning, resulting in abnormalities such as duplication of Mauthner cell and abnormal craniofacial cartilage defects. Crucially, this potentiation effect was abolished by retinoic acid receptor antagonists but not estrogen receptor antagonists, suggesting a direct interaction with RA signaling pathways. Notably, the phenomenon was also observed with other chemicals, indicating a potential generalizable mechanism for a broader range of EDCs. Our findings provide a causal link between chemical exposure and neurodevelopmental impairments, contributing to the potential adverse effects of plastic pollution on development processes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE263569 | GEO | 2025/05/15

REPOSITORIES: GEO

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Project description:Compairsion of transcriptional profiles of heart and skeletal muscle tissue of fetal rhesus monkey exposed to maternal Bisphenol A or vehicle during early or late gestaion. Maternal exposure to the endocrine disrupting chemical, bisphenol A (BPA) affects the development of multiple organ systems in rodents and monkeys. However, effects of BPA exposure on cardiac and skeletal muscle development have not been assessed. Given that maternal BPA crosses placenta and reaches developing fetus, examining the physiological consequences of gestational exposure during development is of research significance. Therefore, we evaluate the effects of daily, oral BPA exposure of pregnant rhesus monkeys (Macaca mulatta) on the fetal heart and skeletal muscle transcriptome. Pregnant monkeys were administered daily oral doses (400 M-BM-5g/kg body weight) of BPA during early (50 M-bM-^@M-^S100 M-BM-1 2 days post conception, dpc) or late (100 M-BM-1 2 dpc - term), gestation. At the end of treatment, fetal heart tissues; left ventricle (LV), right ventricle (RV), left atrium (LA), right atrium (RA) and skeletal muscle; biceps femoris (BFM), were collected. Transcriptome expression was assessed using genome-wide microarray in each of the tissues and compared paired-wise between the BPA and matched control fetuses. Our results show that maternal BPA exposure alters transcriptional profile of several coding and non-coding genes in fetal heart and skeletal muscle. Pregnant rhesus monkey were administered a daily oral dose of 400 M-NM-<g/kg. body weight of Bisphenol A (BPA) or vehicle (CON) either during early (50M-bM-^@M-^S100 M-BM-1 2 days) or late (100 M-BM-1 2 daysM-bM-^@M-^Sterm) gestation. Gene expression profiles of each of the heart chambers (left ventricle, LV; right ventricle, RV; left atrium, LA; and right atrium, RA) and skeletal muscle (biceps femoris, BFM) were analyzed using microarrays and compared between the BPA exposed and matched control fetuses. A total of 12 samples were analyzed for each tissue; LV, RV, LA, RA and BFM. This includes 6 samples at each time period (early vs. late gestation) and 3 biological replicates for each treatment (BPA, n=3; control, n=3).

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Bisphenol A enhances retinoic acid-HOX genes signaling disrupting brain development: human

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