Effects of homocysteine-induced endoplasmic reticulum protein on endoplasmic reticulum stress, autophagy, and neuronal apoptosis following intracerebral hemorrhage
Effects of homocysteine-induced endoplasmic reticulum protein on endoplasmic reticulum stress, autophagy, and neuronal apoptosis following intracerebral hemorrhage
复制标题
同型半胱氨酸诱导的内质网蛋白对脑出血后内质网应激、自噬和神经元凋亡的影响
DOI：
10.1016/j.ibror.2020.08.004
复制
发表时间：
2020-08
期刊：
影响因子：
2.6
通讯作者：
Kaifu Ke
中科院分区：
文献类型：
--
作者：
Hui Wu;Jinglei Wang;Maohong Cao;Jingjing Liang;Dan Wu;Xingxing Gu;Kaifu Ke
脑出血（ICH）是指出血进入脑实质的疾病，具有很高的死亡率和致残率。不幸的是，它仍然是一个未解决的医疗问题。因此，有必要寻找减少脑出血后细胞凋亡的方法。同型半胱氨酸诱导的内质网蛋白（Homocysteine-induced endoplasmic reticulum protein，HERP）是由Herpud 1基因编码的一种早期应激反应蛋白，分子量为54 kD。本研究采用免疫印迹和免疫荧光标记技术，观察了脑出血和氯化血红素刺激后HERP在小鼠和原代皮层神经元中的表达。利用shRNA-HERP质粒和重组腺病毒，我们还研究了HERP如何影响脑出血和氯化血红素刺激后神经细胞凋亡。此外，行为评估是用来确保我们的模型的成功。在体内和体外研究中，HERP的表达增加后，ICH和氯化血红素暴露的原代皮层神经元。HERP耗竭激活内质网（ER）应激途径和细胞凋亡的氯化血红素暴露的原代皮层神经元，但抑制自噬氯化血红素暴露的原代皮层神经元。HERP的过表达抑制ER应激通路和细胞凋亡，但激活自噬在氯化血红素暴露的原代皮层神经元。因此，我们证实HERP在ICH模型中起保护作用。
Intracerebral hemorrhage (ICH) is defined as bleeding into the brain parenchyma with a high mortality and morbidity rate. Unfortunately, it remains an unresolved medical problem. Therefore, it is necessary to find ways to reduce cellular apoptosis after ICH. Homocysteine-induced endoplasmic reticulum protein (HERP), a 54 kD transmembrane protein, is an early stress response protein encoded by ubiquitin-like domain member 1 (Herpud1) gene. In the present work, our group investigated the role of HERP after ICH and hemin stimulation, HERP expression was examined in mouse and primary cortical neurons after ICH and hemin stimulation by western blot and Immunofluorescent labeling. Using shRNA-HERP plasmid and recombinant adenovirus, we also investigated how HERP affected neuronal apoptosis after ICH and hemin stimulation. In addition, behavioral evaluation was used to ensure our models’ success. In vivo and vitro studies, the expression of HERP was increased following ICH and hemin-exposed primary cortical neurons. HERP depletion activated the endoplasmic reticulum (ER) stress pathway and apoptosis in hemin-exposed primary cortical neurons, but inhibited autophagy in hemin-exposed primary cortical neurons. Overexpression of HERP inhibited the ER stress pathway and apoptosis, but activated autophagy in hemin-exposed primary cortical neurons. Consequently, we confirm that HERP plays a protective role in ICH model.
登录
查看更多内容
影响因子：
4.2
作者：
Shi S;Tan P;Yan B;Gao R;Zhao J;Wang J;Guo J;Li N;Ma Z
通讯作者：
Ma Z
影响因子：
4.6
作者：
George AK;Behera J;Kelly KE;Mondal NK;Richardson KP;Tyagi N
通讯作者：
Tyagi N
影响因子：
3.6
作者：
zhao yang;Qingjun Liu;Hui Shi;Xuheng Jiang;Song Wang;Yuanlan Lu;Ji Zhang;Xiaofei Huang;Anyong Yu
通讯作者：
zhao yang;Qingjun Liu;Hui Shi;Xuheng Jiang;Song Wang;Yuanlan Lu;Ji Zhang;Xiaofei Huang;Anyong Yu
影响因子：
5.7
作者：
Jun Yan;Gang Zuo;P. Sherchan;Lei Huang;U. Ocak;Weilin Xu;Zachary D. Travis;Wenna Wang;John H.
通讯作者：
Jun Yan;Gang Zuo;P. Sherchan;Lei Huang;U. Ocak;Weilin Xu;Zachary D. Travis;Wenna Wang;John H.
影响因子：
4.8
作者：
Kokame, K;Agarwala, KL;Miyata, T
通讯作者：
Miyata, T