Impared ER stress caused by deficiency of thyroid hormone receptor

应激增强了RGC细胞的死亡，抑制了神经突起的延长，视网膜胶质细胞在NMDA、NO或缺氧等应激下提高了RGC的存活率。为了探讨应激诱导RGC死亡的机制，我们采用了视网膜胶质细胞DNA微阵列技术。DNA芯片显示，应激条件下，甲状腺激素受体（甲状腺激素受体）显著上调。为探讨TR与RGC存活的关系，通过转染siRNA抑制内源性TR的表达，抑制RGC视网膜胶质细胞的存活率降低。用si RNA敲除TR可增强视网膜胶质细胞中ATF4的表达。这些结果表明，内源性TR可能对RGC中ATF4的表达和细胞凋亡具有重要的调控作用。

The stress enhanced the cell death of RGC and inhibited the prolongation of neurite, and retinal glial cells improve RGC survival under the stress like NMDA, NO or hypoxia. To explore the mechanisms of stress-induced RGC death, DNA microarray of retinal glial cells was used. DNA microarray indicated that thyroid hormone receptor (TR) is significantly upregulated in under the stress. To investigate the association between TR and the survival of RGC, theexpression of endogenous TR was inhibited by transfection with siRNA against TR. The survival rate of RGC cultured with TR supressed retinal glial cells, degreased. Knockout of TR with si RNA enhanced the expression of ATF4 in retinal glial cells. These results indicate that endogenous TR may have an important role for the expression of ATF4 and regulate the apoptosis in RGC.