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首页> 外文期刊>Life sciences >Bone resorption by aryl hydrocarbon receptor-expressing osteoclasts is not disturbed by TCDD in short-term cultures.
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Bone resorption by aryl hydrocarbon receptor-expressing osteoclasts is not disturbed by TCDD in short-term cultures.

机译：在短期培养中，TCDD不会干扰表达芳烃受体的破骨细胞的骨吸收。

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摘要

Polychlorinated dibenzo-p-dioxins (PCDDs) are highly toxic environmental contaminants, and 2,3,7,8-tetrachlorobenzo-p-dioxin (TCDD) is the most potent dioxin. Dioxins bind specifically to the cytosolic aryl hydrocarbon receptor (AHR), which is a ligand-activated transcription factor, and a majority of toxic effects of dioxins are mediated via AHR. We have recently demonstrated that TCDD disrupts bone modeling and decreases bone mechanical strength, and that partial resistance to these effects is related to an altered transactivation domain in AHR structure. In order to better understand the effects of dioxins on bone, we studied the presence and precise localization of AHR and also the number and activity of osteoclasts after TCDD treatments. Total RNA was extracted from mixed bone cell population cultures and expression of AHR mRNA was studied using RT-PCR. Bone cells expressed a considerable amount of AHR mRNA. To see which bone cells express AHR, immunostainings were performed in primary rat bone cell cultures, pure human osteoclast cultures and histological sections from AHR knockout and wild type bones. Immunostaining revealed a strong expression of AHR both in osteoclasts and osteoblasts with an especially prominent stain in bone resorbing osteoclasts. Effects of dioxin on primary bone cells were evaluated after TCDD treatment in the pit formation assay. The activity of osteoclasts was not affected measured as the percentage of active osteoclasts and the actual area of resorbed bone. These data indicate that even though TCDD-treated bones show decreased mechanical strength and size, this is not a direct result from increased osteoclastic bone resorption.
机译：多氯二苯并-对-二恶英（PCDDs）是剧毒的环境污染物，而2,3,7,8-四氯苯并-对-二恶英（TCDD）是最有效的二恶英。二恶英与胞质芳基烃受体（AHR）特异性结合，后者是一个配体激活的转录因子，二恶英的大部分毒性作用是通过AHR介导的。最近，我们证明了TCDD破坏了骨骼的建模并降低了骨骼的机械强度，并且对这些作用的部分抵抗力与AHR结构中反式激活域的改变有关。为了更好地了解二恶英对骨骼的影响，我们研究了AHR的存在和精确定位，以及TCDD处理后破骨细胞的数量和活性。从混合的骨细胞群体培养物中提取总RNA，并使用RT-PCR研究AHR mRNA的表达。骨细胞表达了大量的AHR mRNA。为了观察哪些骨细胞表达AHR，在原代大鼠骨细胞培养物，纯人破骨细胞培养物以及来自AHR敲除和野生型骨的组织学切片中进行了免疫染色。免疫染色显示破骨细胞和成骨细胞均强烈表达AHR，在骨吸收破骨细胞中尤为突出。 TCDD处理后在凹坑形成试验中评估了二恶英对原代骨细胞的影响。破骨细胞的活性不受活性破骨细胞的百分比和吸收骨的实际面积的影响。这些数据表明，尽管经过TCDD处理的骨骼显示出降低的机械强度和尺寸，但这并不是破骨细胞骨吸收增加的直接结果。

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