Core Facility of Gene Engineered Mice, State Key Laboratory of Biotherapy, West China Hospital, West China School of Medicine, Sichuan University, 610041 Chengdu, People's Republic of China.
Mol Cell Biochem. 2010 Jun;339(1-2):155-61. doi: 10.1007/s11010-009-0379-8. Epub 2009 Dec 31.
Trpp5 is one member of the polycystic kidney disease (PKD) family, which belongs to transient receptor potential (TRP) superfamily. Our previous study has shown that Trpp5 is developmentally expressed in mouse testis and overexpression of Trpp5 increases intracellular free calcium concentration in MDCK cells. However, the roles of this protein in cellular processes are largely unknown. Here, we demonstrated that Trpp5 resided in both cytoplasm and cell membrane of HEK293 cells. We found that overexpression of Trpp5 slightly increased the calcium current amplitude of HEK293 cells and shifted the reversal potential to a more negative value. Meanwhile, overexpression of Trpp5 suppressed proliferation of Hela cells via inhibiting DNA replication and induced apoptosis of Hela cells with morphological changes and accumulation of fragmented DNA. Collectively, these findings suggest that Trpp5 might involve calcium homeostasis contributing to cell proliferation and apoptosis.
Trpp5 是多囊肾病 (PKD) 家族的一员，属于瞬时受体电位 (TRP) 超家族。我们之前的研究表明，Trpp5 在小鼠睾丸中呈发育性表达，并且 Trpp5 的过表达会增加 MDCK 细胞中的细胞内游离钙浓度。然而，该蛋白在细胞过程中的作用在很大程度上是未知的。在这里，我们证明 Trpp5 存在于 HEK293 细胞的细胞质和细胞膜中。我们发现 Trpp5 的过表达略微增加了 HEK293 细胞的钙电流幅度，并将反转电位向更负的方向移动。同时，Trpp5 的过表达通过抑制 DNA 复制抑制 Hela 细胞的增殖，并诱导 Hela 细胞发生形态变化和碎片化 DNA 积累的凋亡。总之，这些发现表明 Trpp5 可能参与钙稳态，有助于细胞增殖和凋亡。
