染色体22q11 microRNAs缺失与精神分裂症

Deletion of chromosome 22q11 microRNAs and schizophrenia

关于microRNAs对22q11缺失诱发的精神分裂症的发病机制的研究已成为热门研究的方向之一.22q11缺失导致microRNA介导的异常调节,它已成为精神分裂症的高危因素,主要候选基因是DGCR8和MIR185,DGCR8是参与编码microRNA生物合成必不可少的微处理器;而MIR185编码micro185.22q11缺失症的小鼠模型已经证实了大脑中microRNA生物合成的改变,DGCR8单倍剂量不足可能通过一个特殊的microRNA子集的下调导致了这些改变,MIR185编码的microRNA在前额叶皮质和海马体是高分下调的,而这些脑区是精神分裂症研究的关键脑区.另外,MIR185有两个已经验证的靶基因（RhoA、Cdc42）,这两个基因与精神分裂症中表达水平的改变有关.本文对国内外就染色体22q11microRNAs缺失与精神分裂症关系的文献进行综述.

The research effort has focused on the mircroRNAs and the pathogenesis of schizophrenia induced by 22ql 1 deletion now. The 22ql 1 deletion, which contribut to mircoRNA-mediated dysregulation, is a genetic risk factor for schizophrenia. Primary candidate genes are DGCR8, which encodes a component of the microprocessor complex essential for microRNA biogenesis, and MIR185, which encodes microRNA 185. Mouse models of 22q11. 2DS have demonstrated alterations in brain microRNA biogenesis, and that DGCR8 haploinsufficiency may contribute to these alterations, down regulation of a specific microRNA subset. miR-185 was the top-scoring down-regulated microRNA in both the prefrontal cortex and the hippocampus, brain areas which are the key foci of schizophrenia. In addition, MIR185 has two validated targets （ RhoA, Cdc42）, both of which have been associated with altered expression levels in schizophrenia. In this paper, literatures on deletion of chromosome 22q11 microRNAs and schizophrenia were reviewed.