BMP7 plays a critical role in TMEM100-inhibited cell proliferation and apoptosis in mouse metanephric mesenchymal cells in vitro
BMP7 plays a critical role in TMEM100-inhibited cell proliferation and apoptosis in mouse metanephric mesenchymal cells in vitro
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BMP7 在体外 TMEM100 抑制小鼠后肾间充质细胞增殖和凋亡中发挥关键作用
DOI：
10.1007/s11626-017-0211-9
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发表时间：
2017-12
期刊：
影响因子：
--
通讯作者：
Xie Y.
中科院分区：
文献类型：
--
作者：
Ren D;Ju P;Liu J;Ni D;Gu Y;Long Y;Zhou Q;Xie Y.
肾脏主要来源于后肾间充质细胞（MM细胞）和输尿管芽（UB）的诱导。跨膜蛋白100（transmembrane protein-100，Tmem 100）由两个跨膜区组成，在肾脏发育过程中具有较强的时空表达特征。然而，Tmem 100在小鼠胚胎肾衍生细胞中的功能仍不清楚。我们提供qPCR来验证Tmem 100与BMP信号通路之间的关系。为了阐明Tmem 100在细胞增殖和凋亡中的作用，我们进行了EdU掺入，Annexin V-异硫氰酸荧光素（FITC）凋亡测定。在此，我们发现Tmem 100的敲低增加了小鼠胚肾衍生细胞的增殖和凋亡，并且这种促进作用可以同时被BMP 7的敲低所抑制;这些结果表明BMP 7在Tmem 100调节的细胞增殖和凋亡中起着至关重要的作用。qRT-PCR结果进一步证明Tmem 100的缺陷导致BMP 7的上调，而过度表达可能会得到相反的结果。在BMP 7缺失的MK 3细胞中，Tmem 100高度上调，BMPR-II下调。在BMP 7过表达的MK 3细胞中，Tmem 100的表达降低。在BMPR-II缺失的MK 3细胞中，Tmem 100下调，BMP 7表达保持不变。这些发现表明BMP 7和BMPR-II都可以调节Tmem 100，反之亦然，BMPR-II的表达受BMP 7调节。然而，在MK 3细胞中，BMP 7与BMPR-II没有关联。我们的数据表明，BMP 7在Tmem 100调节细胞增殖和凋亡中的重要作用，并揭示了Tmem 100，BMP 7和BMPR-II在小鼠胚胎肾衍生细胞中的复杂调控网络。
Kidney mainly arises from the induction of metanephric mesenchymal cells (MM cells) and the ureteric bud (UB). Transmembrane protein-100 (Tmem100) consists of two transmembrane regions with strong temporal and spatial expression characteristics during renal development. However, the function of Tmem100 in mouse embryonic kidney-derived cells remained unclear. We provided qPCR to verify the relationship between Tmem100 and the BMP signal pathway. To clarify the role of Tmem100 in cell proliferation and apoptosis, we carry out EdU incorporation, annexin V- fluorescein isothiocyanate (FITC) apoptosis assay. Here, we find that the knockdown of Tmem100 increases the proliferation and apoptosis of mouse embryonic kidney-derived cells, and this promotion can be inhibited by knockdown of BMP7 at the same time; these results suggest that BMP7 plays a crucial role in Tmem100-regulated cell proliferation and apoptosis. qRT-PCR results further demonstrate that the deficiency of Tmem100 leads to BMP7 upregulation and overexpression could get opposite results. In BMP7-depleted MK3 cells, Tmem100 is highly upregulated and BMPR-II is downregulated. And in BMP7-overexpressed MK3 cells, the expression of Tmem100 is decreased. In BMPR-II-depleted MK3 cells, Tmem100 is downregulated and BMP7 expression remains still. These findings indicate that both BMP7 and BMPR-II can regulate Tmem100 and vice versa, and BMPR-II expression is regulated by BMP7. However, BMP7 has no association with BMPR-II in MK3 cells. Our data demonstrated the significant role of BMP7 in Tmem100-regulated cell proliferation and apoptosis and revealed the complicated regulation network among Tmem100, BMP7, and BMPR-II in mouse embryonic kidney-derived cells.
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影响因子：
4.6
作者：
Majumdar, A;Vainio, S;McMahon, AP
通讯作者：
McMahon, AP
影响因子：
12.8
作者：
Hwang, Sung-Min;Jin, MeiHong;Shin, Yong Hwan;Choi, Seul Ki;Namkoong, Eun;Kim, MinKyoung;Park, Moon-Yong;Park, Kyungpyo
通讯作者：
Park, Kyungpyo
跨跨性发育中的凋亡。
DOI：
10.1083/jcb.119.5.1327
发表时间：
1992-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
Koseki C;Herzlinger D;al-Awqati Q
通讯作者：
al-Awqati Q
TMEM100的新作用：抑制肝细胞癌的转移和增殖
影响因子：
--
作者：
Ou D;Yang H;Hua D;Xiao S;Yang L
通讯作者：
Yang L
影响因子：
64.8
作者：
Moore, MW;Klein, RD;Rosenthal, A
通讯作者：
Rosenthal, A