Dexamethasone regulates expression of BRUCE/Apollon and the proliferation of neural progenitor cells
Dexamethasone regulates expression of BRUCE/Apollon and the proliferation of neural progenitor cells
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DOI：
10.1016/j.febslet.2009.06.018
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发表时间：
2009-07
期刊：
影响因子：
3.5
通讯作者：
M. Sippel;R. Rajala;L. Korhonen;B. Bornhauser;A. Sokka;M. Naito;D. Lindholm
中科院分区：
文献类型：
--
作者：
M. Sippel;R. Rajala;L. Korhonen;B. Bornhauser;A. Sokka;M. Naito;D. Lindholm
糖皮质激素（GH）调节神经前体细胞（NPC）的细胞增殖，有助于减少应激后的神经发生。我们在这里表明，地塞米松（Dex）减少布鲁斯/阿波罗（布鲁斯）在培养的NPC中的GH受体依赖性的方式。通过Dex或使用沉默RNA下调布鲁斯减少了增殖的NPC的数量，而布鲁斯的过表达抵消了Dex的作用。Dex还升高了去泛素化酶Usp 8/Ubpy，其通过Nrdp 1降低布鲁斯。结果表明，布鲁斯是NPC中GH的靶点，并且布鲁斯控制NPC的细胞分裂，并且可能控制其他干细胞的细胞分裂。结构性摘要：MINT-7148564：Nrdp 1（uniprotkb：Q8 BH 75）通过抗诱饵免疫共沉淀（MI：0006）与布鲁斯（uniprotkb：O 88738）物理相互作用（MI：0914）MINT-7148555：Nrdp 1（uniprotkb：Q8 BH 75）通过抗诱饵免疫共沉淀（MI：0006）与Usp 8（uniprotkb：Q80 U87）物理相互作用（MI：0914）
Glucocorticoid hormones (GHs) regulate cell proliferation of neural progenitor cells (NPCs) contributing to reduction of neurogenesis after stress. We show here that dexamethasone (Dex) decreases BRUCE/Apollon (BRUCE) in cultured NPCs in a GH-receptor-dependent manner. Downregulation of BRUCE by Dex or using silencing RNA reduced the number of proliferating NPCs, whilst overexpression of BRUCE counteracted the effect of Dex. Dex also elevated the deubiquitinating enzyme, Usp8/Ubpy, which via Nrdp1 decreases BRUCE. The results show that BRUCE is a target for GHs in the NPCs, and that BRUCE controls cell division of NPCs and possibly of other stem cells. STRUCTURED SUMMARY: MINT-7148564: Nrdp1 (uniprotkb:Q8BH75) physically interacts (MI:0914) with BRUCE (uniprotkb:O88738) by anti bait co-immunoprecipitation (MI:0006) MINT-7148555: Nrdp1 (uniprotkb:Q8BH75) physically interacts (MI:0914) with Usp8 (uniprotkb:Q80U87) by anti bait co-immunoprecipitation (MI:0006)