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Circulation:GATA6调节动脉瓣重构,其半剂量效应不足可导致右-左型二叶式主动脉瓣

2018-09-09 MedSci MedSci原创

二叶式主动脉瓣(BAV)是一种常见的先天性心脏缺陷,影响1%-2%的人群,是早期主动脉瓣疾病的主要危险因素,也是大部分换瓣膜的原因。但BAV的病因和发病机制及其遗传基础尚未明确。研究人员对缺失Gata6等位基因的小鼠的心脏结构和功能进行评估,并分析了452例BAV患者和1849位对照的GATA6基因突变。采用定量实时PCR和免疫组化分析GATA6在小鼠和人类组织中的表达量。Gata6杂合小鼠表现为

二叶式主动脉瓣(BAV)是一种常见的先天性心脏缺陷,影响1%-2%的人群,是早期主动脉瓣疾病的主要危险因素,也是大部分换瓣膜的原因。但BAV的病因和发病机制及其遗传基础尚未明确。

研究人员对缺失Gata6等位基因的小鼠的心脏结构和功能进行评估,并分析了452例BAV患者和1849位对照的GATA6基因突变。采用定量实时PCR和免疫组化分析GATA6在小鼠和人类组织中的表达量。

Gata6杂合小鼠表现为高穿透性的右-左(RL)型BAV(在人类患者中最常见的表型)。GATA6在人BAV组织中的转录水平要低于正常的三尖瓣。机制上,Gata6半剂量效应不足通过干扰重要的信号分子(包括机制金属蛋白酶9)破坏瓣膜重构和细胞外基质组成。细胞特异性失活Gata6揭示了GATA6在第二心区的心肌细胞中发挥至关重要的作用,因为Isl-1阳性细胞丢失1个Gata6等位基因可再现Gata6杂合小鼠的表型,但内皮细胞或神经鞘细胞则不能。

总而言之,本研究发现了BAV的新的细胞和分子机制。最常见的人类BAV动物模型的可用性为阐明BAV发病机制和开发急需的治疗开辟了道路。


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    2018-09-11 bbjsj_1981
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    2018-09-09 医者仁心5538

    学习了

    0

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