Cell Stress Chaperones. 2014 Jan;19(1):145-53. doi: 10.1007/s12192-013-0452-9.
Upregulation of small heat-shock proteins (sHsps) in response to cellular stress is one mechanism to increase cell viability.We previously described that cultured rat hippocampal neurons express five of the 11 family members but only upregulate two of them (HspB1 and HspB5) at the protein level after heat stress. Since neurons have to cope with many other pathological conditions, we investigated in this study the expression of all five expressed sHsps on mRNA and protein level after sublethal sodium arsenite and oxidative and hyperosmotic stress. Under all three conditions, HspB1, HspB5, HspB6, and HspB8 but not HspB11 were consistently upregulated but showed differences in the time course of upregulation. The increase of sHsps always occurred earlier on mRNA level compared with protein levels. We conclude from our data that these four upregulated sHsps (HspB1, HspB5, HspB6, HspB8) act together in different proportions in the protection of neurons from various stress conditions.
细胞应激时小热休克蛋白(sHsps)的上调是提高细胞活力的一种机制。我们之前曾描述过,培养的大鼠海马神经元表达 11 个家族成员中的 5 个,但在热应激后仅在蛋白质水平上调其中的 2 个(HspB1 和 HspB5)。由于神经元必须应对许多其他病理状况,因此我们在这项研究中研究了亚致死浓度的砷酸钠以及氧化和高渗应激后所有 5 个表达的 sHsps 在 mRNA 和蛋白质水平上的表达。在这三种情况下,HspB1、HspB5、HspB6 和 HspB8 但不是 HspB11 均一致地上调,但上调的时间过程存在差异。sHsps 的增加总是先于蛋白质水平在 mRNA 水平上发生。我们从数据中得出结论,这四个上调的 sHsps(HspB1、HspB5、HspB6、HspB8)在神经元对各种应激条件的保护中以不同的比例共同作用。