Endoplasmic reticulum stress

Effects of probucol on cultured human umbilical vein endothelial cells injured by hypoxia/reoxygenation

Y. L. Chai, Xu, J. Z., Zhang, Y. L., Sheng, G. T., Chai, Y. L., Xu, J. Z., Zhang, Y. L., and Sheng, G. T., Effects of probucol on cultured human umbilical vein endothelial cells injured by hypoxia/reoxygenation, vol. 15, p. -, 2016.

There is increasing evidence suggesting that endoplasmic reticulum stress (ERS) plays an important role in the initiation and development of atherosclerosis. This study was designed to examine the effect of probucol on cultured human umbilical vein endothelial cells (HUVECs) injured by hypoxia/reoxygenation (H/R) and the potential mechanisms involving ERS. Injured HUVECs induced by Na2S2O4 served as an H/R model in vitro. The concentration of probucol in this study ranged from 3 to 27 μM.

Silencing effect of lentiviral vectors encod­-ing shRNA of Herp on endoplasmic reticulum stress and inflammatory responses in RAW 264.7 macrophages

F. L. Chen, Li, Q., Zhang, J. Y., Lei, L. J., Zhang, Z., Mahmoud, T. N., Wang, X. G., Lin, P. F., Jin, Y. P., and Wang, A. H., Silencing effect of lentiviral vectors encod­-ing shRNA of Herp on endoplasmic reticulum stress and inflammatory responses in RAW 264.7 macrophages, vol. 14, pp. 17587-17598, 2015.

Herp, a mammalian protein with a ubiquitin-like domain, can be strongly upregulated by endoplasmic reticulum (ER) stress during ER-associated protein degradation. However, the other cellular functions of Herp remain unclear. We explored the effect of Herp on ER stress and inflammatory responses in RAW 264.7 macrophages that had been exposed to tunicamycin or thapsigargin. We successfully constructed recombinant lentiviral vectors for Herp short-hairpin RNA (shRNA) expression to better understand the contribution made by Herp to other signaling pathways.

Hypertension-mediated enhancement of JNK activation in association with endoplasmic reticulum stress in rat model hippocampus with cerebral ischemia-reperfusion

Y. N. Zhao, Li, J. M., Chen, C. X., Zhang, P., and Li, S. X., Hypertension-mediated enhancement of JNK activation in association with endoplasmic reticulum stress in rat model hippocampus with cerebral ischemia-reperfusion, vol. 14, pp. 10980-10990, 2015.

Acute brain ischemia can induce the activation of c-Jun N-terminal kinases (JNKs). Hypertension is a critical etiology for brain ischemia. We identified the effects of hypertension on the activation of JNK as well as its impact on SP600125, a JNK inhibitor, during endoplasmic reticulum stress (ERS) in the hippocampus using a rat model. Transient whole-brain ischemia was induced by 4-vessel occlusion (bilateral vertebral and bilateral common carotid arteries) in normal and spontaneous hypertensive rats. SP600125 (0.05 mg/kg, iv) was administered 30 min before ischemia.

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