DLC1 is a focal adhesion molecule that regulates cell polarity, proliferation, migration, and survival. DLC1 functions as a tumor suppressor and its expression is often down-regulated in various malignant neoplasms of epithelial origin. Recent studies have suggested that lack of DLC1 in endothelial cells may contribute to the development of angiosarcoma, and that DLC1 mutations have been identified in patients with nephrotic syndrome, a disease mainly due to leaky glomerular filtration barriers. To demonstrate whether lack of endothelial DLC1 induces angiosarcoma and/or damages glomerular capillaries leading to nephrotic syndrome, we have extended our analyses on endothelial cell-specific DLC1 knockout mice with focuses on their liver and kidney function. Mice were monitored up to 24 months of age. However, no histological or clinical difference was found between DLC1 knockout and wild type mice, indicating that lack of endothelial DLC1 alone does not compromise kidney and liver function in mice.

DLC1 是一种粘着斑分子，可调节细胞极性、增殖、迁移和存活。DLC1 作为肿瘤抑制因子发挥作用，其表达在各种上皮来源的恶性肿瘤中经常下调。最近的研究表明，内皮细胞中 DLC1 的缺乏可能导致血管肉瘤的发展，并且已经在肾病综合征患者中发现了 DLC1 突变，这种疾病主要是由于肾小球滤过屏障渗漏造成的。为了证明缺乏内皮 DLC1 是否会诱发血管肉瘤和/或损害导致肾病综合征的肾小球毛细血管，我们扩展了对内皮细胞特异性 DLC1 敲除小鼠的分析，重点关注其肝肾功能。监测小鼠直至 24 个月大。然而，