Department of Cell Biology, Fukuoka University, Japan.
Cell Mol Biol Lett. 2010 Dec;15(4):541-50. doi: 10.2478/s11658-010-0028-y. Epub 2010 Jul 19.
ZFAT, originally identified as a susceptibility gene for autoimmune thyroid disease, encodes a transcriptional regulator with one AT-hook and 18 C(2)H(2)-type zinc-finger domains. It is highly conserved among species. Here, we demonstrate that ZFAT is clearly expressed in human umbilical vein endothelial cells (HUVECs). Furthermore, we show that endothelial cell assembly and the branch point formation of capillary-like structures in HUVECs is impaired by the reduction of ZFAT expression through the use of ZFAT-miRNAs, whereas differences in cell proliferation or apoptotic features were not observed after the reduction in ZFAT expression. These results suggest that ZFAT may have critical roles in the capillary-like network formation that is involved in vascular remodeling. Elucidating the ZFAT-mediated transcriptional network will lead to a better understanding of the molecular mechanisms of angiogenesis.
ZFAT,最初被鉴定为自身免疫性甲状腺疾病的易感基因,编码一种转录调节剂,具有一个 AT 钩和 18 个 C(2)H(2)-型锌指结构域。它在物种间高度保守。在这里,我们证明 ZFAT 在人脐静脉内皮细胞 (HUVEC) 中明显表达。此外,我们通过使用 ZFAT-miRNA 显示,ZFAT 表达的减少会损害内皮细胞的组装和 HUVEC 中毛细血管样结构的分支点形成,而在 ZFAT 表达减少后,细胞增殖或凋亡特征没有差异。这些结果表明,ZFAT 可能在参与血管重塑的毛细血管样网络形成中具有关键作用。阐明 ZFAT 介导的转录网络将有助于更好地理解血管生成的分子机制。