用双A,双F,双S和双AF对参与骨形成和再吸收的标记物的基因表达调节
Enrique García-Recio1,2, Anabel González-Acedo1,2, Francisco Javier Manzano-Moreno1,3
1Biomedical Group (BIO277), Department of Nursing, Faculty of Health Sciences, University of Granada, Avda. Ilustración 60, 18016 Granada, Spain.
Genes
|November 27, 2024
概括
双化合物 (BPA,BPF,BPS,BPAF) 通过改变关键生长因子,如VEGF和TGF-β1.1,对骨细胞产生负面影响. 这些变化表明双醇诱导的骨损伤机制,独立于骨质细胞形成.
科学领域:
- 内分泌学 在内分泌学.
- 毒理学 毒理学 毒理学
- 骨生物学 骨生物学 骨生物学
背景情况:
- 双甲 (BPA) 和其类似物 (BPF,BPS,BPAF) 是内分泌干扰化学物质,已知对骨组织有不良影响.
- 这些化合物在消费品中广泛使用,导致人类潜在暴露和健康问题.
研究的目的:
- 调查BPA及其类似物对骨质细胞基因表达的影响.
- 分析骨信息和修复中的关键因素的影响:VEGF,TGF-β1和TGF-β受体 (TGFR1,TGFR2,TGFR3).
主要方法:
- 人类骨质芽细胞在24小时内用不同剂量的BPA,BPF,BPS或BPAF培养 (10-5至10-7M).
- 使用RT-PCR量化了RANKL,OPG,TGF-β1,TGFR1,TGFR2,TGFR3和VEGF的基因表达.
主要成果:
- 所有测试的双,除了BPAF,下调RANKL和OPG表达剂量依赖的方式.
- 在BPAF上调的OPG表达式.
- 所有双都对TGF-β1及其受体表达进行了下调.
- VEGF表达被BPF,BPAF和BPA (在较高剂量下) 下调,但不是BPS.
结论:
- 双诱导的RANKL和OPG的下调表明,骨质细胞形成的增加不是骨损伤的主要机制.
- 观察到TGF-β1,TGF-β受体和骨质母细胞中VEGF表达的变化表明显著的分子变化导致双诱导的骨毒性.
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