scholarly journals Third trimester phthalate exposure is associated with DNA methylation of growth-related genes in human placenta

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yan Zhao ◽  
Jiao Chen ◽  
Xiu Wang ◽  
Qi Song ◽  
Hui-Hui Xu ◽  
...  
2014 ◽  
Vol 56 (3) ◽  
pp. 286-292 ◽  
Author(s):  
Yan Zhao ◽  
Hui-jing Shi ◽  
Chang-ming Xie ◽  
Jiao Chen ◽  
Hannah Laue ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wan-Ru Wang ◽  
Nai-Tzu Chen ◽  
Nai-Yun Hsu ◽  
I-Ying Kuo ◽  
Hsin-Wen Chang ◽  
...  

Abstract Background Dysregulation of thymic stromal lymphopoietin (TSLP) expressions is linked to asthma and allergic disease. Exposure to phthalate esters, a widely used plasticizer, is associated with respiratory and allergic morbidity. Dibutyl phthalate (DBP) causes TSLP upregulation in the skin. In addition, phthalate exposure is associated with changes in environmentally induced DNA methylation, which might cause phenotypic heterogeneity. This study examined the DNA methylation of the TSLP gene to determine the potential mechanism between phthalate exposure and allergic diseases. Results Among all evaluated, only benzyl butyl phthalate (BBzP) in the settled dusts were negatively correlated with the methylation levels of TSLP and positively associated with children’s respiratory symptoms. The results revealed that every unit increase in BBzP concentration in the settled dust was associated with a 1.75% decrease in the methylation level on upstream 775 bp from the transcription start site (TSS) of TSLP (β =  − 1.75, p = 0.015) after adjustment for child’s sex, age, BMI, parents’ smoking status, allergic history, and education levels, PM2.5, formaldehyde, temperature; and relative humidity. Moreover, every percentage increase in the methylation level was associated with a 20% decrease in the risk of morning respiratory symptoms in the children (OR 0.80, 95% CI 0.65–0.99). Conclusions Exposure to BBzP in settled dust might increase children’s respiratory symptoms in the morning through decreasing TSLP methylation. Therefore, the exposure to BBzP should be reduced especially for the children already having allergic diseases.


Epigenetics ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. 333-337 ◽  
Author(s):  
Kirsten Hogg ◽  
E Magda Price ◽  
Wendy P Robinson

2020 ◽  
Vol 737 ◽  
pp. 139833
Author(s):  
Chia-Huang Chang ◽  
Chian-Feng Chen ◽  
Yen-An Tsai ◽  
Shu-Li Wang ◽  
Po-Chin Huang ◽  
...  

1986 ◽  
Vol 14 (21) ◽  
pp. 8387-8397 ◽  
Author(s):  
Xian-Yang Zhang ◽  
Kenneth C. Ehrlich ◽  
Richard Y.-H. Wang ◽  
Melanie Ehrlich

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Angela Lucariello ◽  
Angelica Perna ◽  
Carmine Sellitto ◽  
Alfonso Baldi ◽  
Alessandro Iannaccone ◽  
...  

TheWFS1gene, encoding a transmembrane glycoprotein of the endoplasmic reticulum called wolframin, is mutated in Wolfram syndrome, an autosomal recessive disorder defined by the association of diabetes mellitus, optic atrophy, and further organ abnormalities. Disruption of theWFS1gene in mice causes progressiveβ-cell loss in the pancreas and impaired stimulus-secretion coupling in insulin secretion. However, little is known about the physiological functions of this protein. We investigated the immunohistochemical expression of wolframin in human placenta throughout pregnancy in normal women and diabetic pregnant women. In normal placenta, there was a modulation of wolframin throughout pregnancy with a strong level of expression during the first trimester and a moderate level in the third trimester of gestation. In diabetic women, wolframin expression was strongly reduced in the third trimester of gestation. The pattern of expression of wolframin in normal placenta suggests that this protein may be required to sustain normal rates of cytotrophoblast cell proliferation during the first trimester of gestation. The decrease in wolframin expression in diabetic placenta suggests that this protein may participate in maintaining the physiologic glucose homeostasis in this organ.


2012 ◽  
Vol 120 (2) ◽  
pp. 296-302 ◽  
Author(s):  
Charlotte S. Wilhelm-Benartzi ◽  
E. Andres Houseman ◽  
Matthew A. Maccani ◽  
Graham M. Poage ◽  
Devin C. Koestler ◽  
...  

2016 ◽  
Vol 64 (12) ◽  
pp. 769-784 ◽  
Author(s):  
Tina Storm ◽  
Erik I. Christensen ◽  
Julie Nelly Christensen ◽  
Tine Kjaergaard ◽  
Niels Uldbjerg ◽  
...  

The membrane receptor megalin is crucial for normal fetal development. Besides its expression in the developing fetus, megalin is also expressed in the human placenta. Similar to its established function in the kidney proximal tubules, placental megalin has been proposed to mediate uptake of vital nutrients. However, details of megalin expression, subcellular localization, and function in the human placenta remain to be established. By immunohistochemical analyses of first trimester and term human placenta, we showed that megalin is predominantly expressed in cytotrophoblasts, the highly proliferative cells in placenta. Only limited amounts of megalin could be detected in syncytiotrophoblasts and least in term placenta syncytiotrophoblasts. Immunocytochemical analyses furthermore showed that placental megalin associates with structures of the endolysosomal apparatus. Combined, our results clearly place placental megalin in the context of endocytosis and trafficking of ligands. However, due to the limited expression of megalin in syncytiotrophoblasts, especially in term placenta, it appears that the main role for placental megalin is not to mediate uptake of nutrients from the maternal bloodstream, as previously proposed. In contrast, our results point toward novel and complex functions for megalin in the cytotrophoblasts. Thus, we propose that the perception of placental megalin localization and function should be revised.


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