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RASA1:伴有毛细血管和动静脉畸形的可变表型。

RASA1: variable phenotype with capillary and arteriovenous malformations.

作者信息

Boon Laurence M, Mulliken John B, Vikkula Miikka

机构信息

Laboratory of Human Molecular Genetics, Christian de Duve Institute of Cellular Pathology and University of Louvain Medical School, Brussels, Belgium.

出版信息

Curr Opin Genet Dev. 2005 Jun;15(3):265-9. doi: 10.1016/j.gde.2005.03.004.

Abstract

Capillary malformation-arteriovenous malformation (CM-AVM) is a newly discovered hereditary disorder. Its defining features are atypical cutaneous multifocal capillary malformations often in association with high-flow lesions: cutaneous, subcutaneous, intramuscular, intraosseous and cerebral arteriovenous malformations and arteriovenous fistulas. Some patients have Parkes Weber syndrome - a large congenital cutaneous vascular stain in an extremity, with bony and soft tissue hypertrophy and microscopic arteriovenous shunting. In the past, arteriovenous malformations and arteriovenous fistulas had been considered non-hereditary. A classical genetic approach was used to identify the locus. Candidate gene screening pinpointed mutations in RASA1 (p120-RASGAP) - a RasGTPase. RASA1 reverts active GTP-bound Ras into inactive GDP-bound form. Murine Rasa1 knockout and tetraploid-aggregated embryos with RNA interference exhibited abnormal vascular development. Lack of RASA1 activity caused inhibition of cell motility, possibly through p190-RhoGAP. Thus, RASA1 defects probably cause abnormal angiogenic remodeling of the primary capillary plexus that cannot be compensated for by other RasGAPs: RASA2, RASAL and NF1. Signaling pathways involving RASA1 might offer novel targets for treatment of high-flow vascular anomalies.

摘要

毛细血管畸形 - 动静脉畸形(CM - AVM)是一种新发现的遗传性疾病。其特征性表现为非典型的皮肤多灶性毛细血管畸形,常伴有高流量病变:皮肤、皮下、肌肉内、骨内和脑动静脉畸形以及动静脉瘘。一些患者患有帕克斯·韦伯综合征——肢体上有一个大的先天性皮肤血管斑,伴有骨和软组织肥大以及微小动静脉分流。过去,动静脉畸形和动静脉瘘被认为是非遗传性的。采用经典的遗传学方法来确定基因座。候选基因筛查确定了RASA1(p120 - RASGAP)——一种RasGTP酶中的突变。RASA1将活性的GTP结合型Ras转化为无活性的GDP结合型。小鼠Rasa1基因敲除和RNA干扰的四倍体聚集胚胎表现出异常的血管发育。RASA1活性的缺乏可能通过p190 - RhoGAP导致细胞运动受到抑制。因此,RASA1缺陷可能导致初级毛细血管丛的血管生成重塑异常,而其他RasGAP(RASA2、RASAL和NF1)无法对此进行补偿。涉及RASA1的信号通路可能为治疗高流量血管异常提供新的靶点。

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