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Journal articles on the topic 'Endoplasmic reticulum stress'

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Author: Grafiati

Published: 4 June 2021

Last updated: 6 July 2024

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1

BANHEGYI, G., P. BAUMEISTER, A. BENEDETTI, D. DONG, Y. FU, A. S. LEE, J. LI, et al. "Endoplasmic Reticulum Stress." Annals of the New York Academy of Sciences 1113, no. 1 (May 18, 2007): 58–71. http://dx.doi.org/10.1196/annals.1391.007.

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2

Schröder, M. "Endoplasmic reticulum stress responses." Cellular and Molecular Life Sciences 65, no. 6 (November 26, 2007): 862–94. http://dx.doi.org/10.1007/s00018-007-7383-5.

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3

HAN, Sevtap, Mecit Orhan ULUDAĞ, and Emine DEMİREL YILMAZ. "Endoplasmic Reticulum Stress and Hypertension." Turkiye Klinikleri Journal of Internal Medicine 4, no. 3 (2019): 147–53. http://dx.doi.org/10.5336/intermed.2019-65618.

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4

Hu, Yanan, Wenhao Yang, Liang Xie, Tao Liu, Hanmin Liu, and Bin Liu. "Endoplasmic reticulum stress and pulmonary hypertension." Pulmonary Circulation 10, no. 1 (January 2020): 204589401990012. http://dx.doi.org/10.1177/2045894019900121.

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Pulmonary hypertension is a fatal disease of which pulmonary vasculopathy is the main pathological feature resulting in the mean pulmonary arterial pressure higher than 25 mmHg. Moreover, pulmonary hypertension remains a tough problem with unclear molecular mechanisms. There have been dozens of studies about endoplasmic reticulum stress during the onset of pulmonary hypertension in patients, suggesting that endoplasmic reticulum stress may have a critical effect on the pathogenesis of pulmonary hypertension. The review aims to summarize the rationale to elucidate the role of endoplasmic reticulum stress in pulmonary hypertension. Started by reviewing the mechanisms responsible for the unfolded protein response following endoplasmic reticulum stress, the potential link between endoplasmic reticulum stress and pulmonary hypertension were introduced, and the contributions of endoplasmic reticulum stress to different vascular cells, mitochondria, and inflammation were described, and finally the potential therapies of attenuating endoplasmic reticulum stress for pulmonary hypertension were discussed.

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5

Koch, G., M. Smith, D. Macer, P. Webster, and R. Mortara. "Endoplasmic reticulum contains a common, abundant calcium-binding glycoprotein, endoplasmin." Journal of Cell Science 86, no. 1 (December 1, 1986): 217–32. http://dx.doi.org/10.1242/jcs.86.1.217.

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The most abundant protein in microsomal membrane preparations from mammalian cells has been identified as a 100 X 10(3) Mr concanavalin A-binding glycoprotein. The glycosyl moiety of the glycoprotein is completely sensitive to endoglycosidase H, suggesting a predominantly endoplasmic reticulum localization in the cell. Using a monospecific antibody it was shown by binding and immunofluorescence studies that the glycoprotein is intracellular. Immunoelectron microscopy showed that the glycoprotein was at least 100 times more concentrated in the endoplasmic reticulum than in any other cellular organelle. It was found to be substantially overexpressed in cells and tissues rich in endoplasmic reticulum. Since it is the major common protein component associated with the endoplasmic reticulum we refer to it as endoplasmin. Calcium-binding studies show that endoplasmin is a major calcium-binding protein in cells, suggesting that at least one of its roles might be in the calcium-storage function of the endoplasmic reticulum. The amino-terminal sequence of endoplasmin is identical to that of a 100 X 10(3) Mr stress-related protein.

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6

Groenendyk, Jody, Xiao Fan, Zhenling Peng, Lukasz Kurgan, and Marek Michalak. "Endoplasmic reticulum and the microRNA environment in the cardiovascular system." Canadian Journal of Physiology and Pharmacology 97, no. 6 (June 2019): 515–27. http://dx.doi.org/10.1139/cjpp-2018-0720.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in the biology of the cardiac myocyte, and are involved in pathological cardiac function and remodeling. In this paper, we review a link between endoplasmic reticulum homeostasis and microRNA with an emphasis on the impact on stress responses in the cardiovascular system.

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7

Das, Swapan K., Winston S. Chu, Ashis K. Mondal, Neeraj K. Sharma, Philip A. Kern, Neda Rasouli, and Steven C. Elbein. "Effect of pioglitazone treatment on endoplasmic reticulum stress response in human adipose and in palmitate-induced stress in human liver and adipose cell lines." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E393—E400. http://dx.doi.org/10.1152/ajpendo.90355.2008.

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Obesity and elevated cytokine secretion result in a chronic inflammatory state and may cause the insulin resistance observed in type 2 diabetes. Recent studies suggest a key role for endoplasmic reticulum stress in hepatocytes and adipocytes from obese mice, resulting in reduced insulin sensitivity. To address the hypothesis that thiazolidinediones, which improve peripheral insulin sensitivity, act in part by reducing the endoplasmic reticulum stress response, we tested subcutaneous adipose tissue from 20 obese volunteers treated with pioglitazone for 10 wk. We also experimentally induced endoplasmic reticulum stress using palmitate, tunicamycin, and thapsigargin in the human HepG2 liver cell line with or without pioglitazone pretreatment. We quantified endoplasmic reticulum stress response by measuring both gene expression and phosphorylation. Pioglitazone significantly improved insulin sensitivity in human volunteers ( P = 0.002) but did not alter markers of endoplasmic reticulum stress. Differences in pre- and posttreatment endoplasmic reticulum stress levels were not correlated with changes in insulin sensitivity or body mass index. In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2α, JNK1, and c- jun. Although patterns of endoplasmic reticulum stress response differed among palmitate, tunicamycin, and thapsigargin, pioglitazone pretreatment had no significant effect on any measure of endoplasmic reticulum stress, regardless of the inducer. Together, our data suggest that improved insulin sensitivity with pioglitazone is not mediated by a reduction in endoplasmic reticulum stress.

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8

Hadley, Gina, Ain A. Neuhaus, Yvonne Couch, Daniel J. Beard, Bryan A. Adriaanse, Kostas Vekrellis, Gabriele C. DeLuca, Michalis Papadakis, Brad A. Sutherland, and Alastair M. Buchan. "The role of the endoplasmic reticulum stress response following cerebral ischemia." International Journal of Stroke 13, no. 4 (August 4, 2017): 379–90. http://dx.doi.org/10.1177/1747493017724584.

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Background Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability . Methods In vivo: male Wistar rats underwent sham or 10 min of transient global cerebral ischemia. CA1 and CA3 areas were microdissected and endoplasmic reticulum stress protein expression quantified at 3 h and 12 h of reperfusion. In vitro: primary neuronal cultures (E18 Wistar rat embryos) were exposed to 2 h of oxygen and glucose deprivation or normoxia in the presence of an endoplasmic reticulum stress inducer (thapsigargin or tunicamycin), an endoplasmic reticulum stress inhibitor (salubrinal or 4-phenylbutyric acid), an autophagy inducer ([4′-(N-diethylamino) butyl]-2-chlorophenoxazine (10-NCP)) or autophagy inhibitor (3-methyladenine). Results In vivo, decreased endoplasmic reticulum stress protein expression (phospho-eIF2α and ATF4) was observed at 3 h of reperfusion in CA3 neurons following ischemia, and increased in CA1 neurons at 12 h of reperfusion. In vitro, endoplasmic reticulum stress inducers and high doses of the endoplasmic reticulum stress inhibitors also increased cell death. Both induction and inhibition of autophagy also increased cell death. Conclusion Endoplasmic reticulum stress is associated with neuronal cell death following ischemia. Neither reduction of endoplasmic reticulum stress nor induction of autophagy demonstrated neuroprotection in vitro, highlighting their complex role in neuronal biology following ischemia.

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9

Zhou, Long-Xia, An-Ning Yang, Jiu-Kai Chen, Li Zhao, Yan-Hua Wang, Xian-Mei Liu, Xin Cai, Ming-Hao Zhang, Yi-Deng Jiang, and Jun Cao. "Endoplasmic reticulum oxidoreductin 1α mediates homocysteine-induced hepatocyte endoplasmic reticulum stress." World Chinese Journal of Digestology 22, no. 34 (2014): 5228. http://dx.doi.org/10.11569/wcjd.v22.i34.5228.

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10

Alam, Rashedul, Mohammad Mamun Ur Rashid, Mohammad Fazlul Kabir, and Hyung-Ryong Kim. "Endoplasmic reticulum stress and organoids." Organoid 1 (January 31, 2021): e3. http://dx.doi.org/10.51335/organoid.2021.1.e3.

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Organoids represent an advanced tool in cell biology and have redefined biomedical research. Organoids are ideal for studies of biological processes, pharmacological studies, and therapeutic research to imitate pathological processes and preserve genetic integrity. The endoplasmic reticulum (ER) is the central organelle responsible for protein folding, post-translational adaptations, and membrane and luminal protein transportation. ER stress is a disorder influenced by a range of physiological and pathological causes, such as nutrient deficiency, impaired glycosylation, calcium depletion, oxidative stress, DNA damage, and energy disruption. Disturbance of the ER environment triggers aggregation of unfolded/misfolded proteins, accelerating ER stress. The unfolded protein response (UPR) is a transduction mechanism that activates cells in response to ER stress to restore ER homeostasis, altering cancer development and progression. However, the mechanisms through which sustained and unresolved UPR signaling triggers a switch from pro-survival to pro-death pathways remain unclear. Immutable and environmental stimuli that modify protein homeostasis are often incorporated into tumor cells, thereby generating ER stress. Herein, we discuss challenges and advances in fundamental and clinical cancer studies on ER stress. Additionally, current trends in organoid technology are summarized to fill the gap in our knowledge of the relationship between cancer and ER stress, with the UPR representing a future tool for investigating drug response screening and potentially revolutionizing the workflow of new cancer drug development.

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11

CHANG, YanZhong, PeiNa WANG, and YuanYuan LIU. "Ferroptosis and endoplasmic reticulum stress." SCIENTIA SINICA Vitae 51, no. 2 (September 1, 2020): 126–34. http://dx.doi.org/10.1360/ssv-2020-0116.

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12

Kim, Mi Kyung, and Keun Gyu Park. "Endoplasmic Reticulum Stress and Diabetes." Journal of Korean Endocrine Society 23, no. 1 (2008): 1. http://dx.doi.org/10.3803/jkes.2008.23.1.1.

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13

Yadav, Raj Kumar, Soo-Wan Chae, Hyung-Ryong Kim, and Han Jung Chae. "Endoplasmic Reticulum Stress and Cancer." Journal of Cancer Prevention 19, no. 2 (June 30, 2014): 75–88. http://dx.doi.org/10.15430/jcp.2014.19.2.75.

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14

Zhou, Junzhi, Beibei Mao, Qi Zhou, Deqiang Ding, Miao Wang, Peng Guo, Yuhao Gao, Jerry W. Shay, Zengqiang Yuan, and Yu-Sheng Cong. "Endoplasmic reticulum stress activates telomerase." Aging Cell 13, no. 1 (October 22, 2013): 197–200. http://dx.doi.org/10.1111/acel.12161.

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15

Crouser, Elliott D. "Sepsis-Induced Endoplasmic Reticulum Stress." Critical Care Medicine 44, no. 8 (August 2016): 1626–27. http://dx.doi.org/10.1097/ccm.0000000000001694.

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16

Hotamisligil, Gökhan S. "Endoplasmic reticulum stress and atherosclerosis." Nature Medicine 16, no. 4 (April 2010): 396–99. http://dx.doi.org/10.1038/nm0410-396.

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17

Minchenko, DO, KI Kubaĭchuk, OV Hubenia, IV Kryvdiuk, IeV Khomenko, RM Herasymenko, RV Sulik, NK Murashko, and OH Minchenko. "Endoplasmic reticulum stress and angiogenesis." Fiziolohichnyĭ zhurnal 59, no. 4 (August 15, 2013): 93–106. http://dx.doi.org/10.15407/fz59.04.093.

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18

Yorimitsu, Tomohiro, Usha Nair, Zhifen Yang, and Daniel J. Klionsky. "Endoplasmic Reticulum Stress Triggers Autophagy." Journal of Biological Chemistry 281, no. 40 (August 10, 2006): 30299–304. http://dx.doi.org/10.1074/jbc.m607007200.

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19

Khan, Mohammad Moshahid, Weng-Lang Yang, and Ping Wang. "ENDOPLASMIC RETICULUM STRESS IN SEPSIS." Shock 44, no. 4 (October 2015): 294–304. http://dx.doi.org/10.1097/shk.0000000000000425.

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20

SATO, Masao, and Shinya SUZUKI. "Endoplasmic Reticulum Stress and Metallothionein." YAKUGAKU ZASSHI 127, no. 4 (April 1, 2007): 703–8. http://dx.doi.org/10.1248/yakushi.127.703.

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21

Li, Jianze, Brenda Lee, and Amy S. Lee. "Endoplasmic Reticulum Stress-induced Apoptosis." Journal of Biological Chemistry 281, no. 11 (January 6, 2006): 7260–70. http://dx.doi.org/10.1074/jbc.m509868200.

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22

Kraskiewicz, Honorata, and Una FitzGerald. "InterfERing with endoplasmic reticulum stress." Trends in Pharmacological Sciences 33, no. 2 (February 2012): 53–63. http://dx.doi.org/10.1016/j.tips.2011.10.002.

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23

Bettigole, Sarah E., and Laurie H. Glimcher. "Endoplasmic Reticulum Stress in Immunity." Annual Review of Immunology 33, no. 1 (March 21, 2015): 107–38. http://dx.doi.org/10.1146/annurev-immunol-032414-112116.

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24

Clarke, Hanna J., Joseph E. Chambers, Elizabeth Liniker, and Stefan J. Marciniak. "Endoplasmic Reticulum Stress in Malignancy." Cancer Cell 25, no. 5 (May 2014): 563–73. http://dx.doi.org/10.1016/j.ccr.2014.03.015.

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25

Hama, Taketsugu, Koichi Nakanishi, Hironobu Mukaiyama, Masashi Sato, Yuko Shima, and Norishige Yoshikawa. "Cyclosporine and endoplasmic reticulum stress." Nihon Shoni Jinzobyo Gakkai Zasshi 27, no. 1 (2014): 13–18. http://dx.doi.org/10.3165/jjpn.27.13.

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26

TAKAHASHI, RYOSUKE, YUZURU IMAI, NOBUTAKA HATTORI, and YOSHIKUNI MIZUNO. "Parkin and Endoplasmic Reticulum Stress." Annals of the New York Academy of Sciences 991, no. 1 (January 24, 2006): 101–6. http://dx.doi.org/10.1111/j.1749-6632.2003.tb07467.x.

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27

Zhou, Huiping, Lixin Sun, Jian Xiao, Luyong Zhang, Xiaokun Li, Elaine Studer, William Pandak, and Phillip Hylemon. "Endoplasmic Reticulum Stress and Atherosclerosis." Current Hypertension Reviews 6, no. 1 (February 1, 2010): 66–71. http://dx.doi.org/10.2174/157340210790231744.

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28

Adolph, Timon-Eric, Lukas Niederreiter, Richard S. Blumberg, and Arthur Kaser. "Endoplasmic Reticulum Stress and Inflammation." Digestive Diseases 30, no. 4 (2012): 341–46. http://dx.doi.org/10.1159/000338121.

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29

Miyata, Toshio, Reiko Inagi, Satoshi Sugiyama, and Nobuteru Usuda. "Serpinopathy and endoplasmic reticulum stress." Medical Molecular Morphology 38, no. 2 (June 10, 2005): 73–78. http://dx.doi.org/10.1007/s00795-004-0281-0.

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30

Martinez, Alexis, Cristian M. Lamaizon, Cristian Valls, Fabien Llambi, Nancy Leal, Patrick Fitzgerald, Cliff Guy, et al. "c-Abl Phosphorylates MFN2 to Regulate Mitochondrial Morphology in Cells under Endoplasmic Reticulum and Oxidative Stress, Impacting Cell Survival and Neurodegeneration." Antioxidants 12, no. 11 (November 16, 2023): 2007. http://dx.doi.org/10.3390/antiox12112007.

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The endoplasmic reticulum is a subcellular organelle key in the control of synthesis, folding, and sorting of proteins. Under endoplasmic reticulum stress, an adaptative unfolded protein response is activated; however, if this activation is prolonged, cells can undergo cell death, in part due to oxidative stress and mitochondrial fragmentation. Here, we report that endoplasmic reticulum stress activates c-Abl tyrosine kinase, inducing its translocation to mitochondria. We found that endoplasmic reticulum stress-activated c-Abl interacts with and phosphorylates the mitochondrial fusion protein MFN2, resulting in mitochondrial fragmentation and apoptosis. Moreover, the pharmacological or genetic inhibition of c-Abl prevents MFN2 phosphorylation, mitochondrial fragmentation, and apoptosis in cells under endoplasmic reticulum stress. Finally, in the amyotrophic lateral sclerosis mouse model, where endoplasmic reticulum and oxidative stress has been linked to neuronal cell death, we demonstrated that the administration of c-Abl inhibitor neurotinib delays the onset of symptoms. Our results uncovered a function of c-Abl in the crosstalk between endoplasmic reticulum stress and mitochondrial dynamics via MFN2 phosphorylation.

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31

Li, Yina, Mingyang Li, Shi Feng, Qingxue Xu, Xu Zhang, Xiaoxing Xiong, and Lijuan Gu. "Ferroptosis and endoplasmic reticulum stress in ischemic stroke." Neural Regeneration Research 19, no. 3 (July 20, 2023): 611–18. http://dx.doi.org/10.4103/1673-5374.380870.

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Abstract Ferroptosis is a form of non-apoptotic programmed cell death, and its mechanisms mainly involve the accumulation of lipid peroxides, imbalance in the amino acid antioxidant system, and disordered iron metabolism. The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum, and the progression of inflammatory diseases can trigger endoplasmic reticulum stress. Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival. Ferroptosis and endoplasmic reticulum stress may occur after ischemic stroke. However, there are few reports on the interactions of ferroptosis and endoplasmic reticulum stress with ischemic stroke. This review summarized the recent research on the relationships between ferroptosis and endoplasmic reticulum stress and ischemic stroke, aiming to provide a reference for developing treatments for ischemic stroke.

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32

Yang, Wei, and Wulf Paschen. "Unfolded protein response in brain ischemia: A timely update." Journal of Cerebral Blood Flow & Metabolism 36, no. 12 (October 14, 2016): 2044–50. http://dx.doi.org/10.1177/0271678x16674488.

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Folding and processing newly synthesized proteins are vital functions of the endoplasmic reticulum that are sensitive to a variety of stress conditions. The unfolded protein response is activated to restore endoplasmic reticulum function impaired by stress. While we know that brain ischemia impairs endoplasmic reticulum function, the role of unfolded protein response activation in post-ischemic recovery of neurologic function is only beginning to emerge. Here, we summarize what is known about endoplasmic reticulum stress and unfolded protein response in brain ischemia and discuss recent findings from myocardial ischemia studies that could help to advance research on endoplasmic reticulum stress and unfolded protein response in brain ischemia.

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HAN, Fang, Hong LIU, Bing XIAO, Dongjuan LIU, Lili WEN, Wei ZHAO, Fanzhen KONG, Dongmei ZHAO, Xiaoyan LI, and Yuxiu SHI. "Endoplasmic reticulum stress and posttraumatic stress disorder." Advances in Psychological Science 25, no. 12 (2017): 2013. http://dx.doi.org/10.3724/sp.j.1042.2017.02013.

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34

Liang, Wu-Lin, Meng-Ru Cai, Ming-Qian Zhang, Shuang Cui, Tian-Rui Zhang, Wen-Hao Cheng, Yong-Hong Wu, Wen-Jing Ou, Zhan-Hong Jia, and Shuo-Feng Zhang. "Chinese Herbal Medicine Alleviates Myocardial Ischemia/Reperfusion Injury by Regulating Endoplasmic Reticulum Stress." Evidence-Based Complementary and Alternative Medicine 2021 (December 7, 2021): 1–17. http://dx.doi.org/10.1155/2021/4963346.

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Myocardial ischemia/reperfusion injury is the main cause of increased mortality and disability in cardiovascular diseases. The injury involves many pathological processes, such as oxidative stress, calcium homeostasis imbalance, inflammation, and energy metabolism disorders, and these pathological stimuli can activate endoplasmic reticulum stress. In the early stage of ischemia, endoplasmic reticulum stress alleviates the injury as an adaptive survival response, but the long-term stress on endoplasmic reticulum amplifies oxidative stress, inflammation, and calcium overload to accelerate cell damage and apoptosis. Therefore, regulation of endoplasmic reticulum stress may be a mechanism to improve ischemia/reperfusion injury. Chinese herbal medicine has a long history of clinical application and unique advantages in the treatment of ischemic heart diseases. This review focuses on the effect of Chinese herbal medicine on myocardial ischemia/reperfusion injury from the perspective of regulation of endoplasmic reticulum stress.

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35

Correia de Sousa, Marta, Etienne Delangre, Miranda Türkal, Michelangelo Foti, and Monika Gjorgjieva. "Endoplasmic Reticulum Stress in Renal Cell Carcinoma." International Journal of Molecular Sciences 24, no. 5 (March 3, 2023): 4914. http://dx.doi.org/10.3390/ijms24054914.

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The endoplasmic reticulum is an organelle exerting crucial functions in protein production, metabolism homeostasis and cell signaling. Endoplasmic reticulum stress occurs when cells are damaged and the capacity of this organelle to perform its normal functions is reduced. Subsequently, specific signaling cascades, together forming the so-called unfolded protein response, are activated and deeply impact cell fate. In normal renal cells, these molecular pathways strive to either resolve cell injury or activate cell death, depending on the extent of cell damage. Therefore, the activation of the endoplasmic reticulum stress pathway was suggested as an interesting therapeutic strategy for pathologies such as cancer. However, renal cancer cells are known to hijack these stress mechanisms and exploit them to their advantage in order to promote their survival through rewiring of their metabolism, activation of oxidative stress responses, autophagy, inhibition of apoptosis and senescence. Recent data strongly suggest that a certain threshold of endoplasmic reticulum stress activation needs to be attained in cancer cells in order to shift endoplasmic reticulum stress responses from a pro-survival to a pro-apoptotic outcome. Several endoplasmic reticulum stress pharmacological modulators of interest for therapeutic purposes are already available, but only a handful were tested in the case of renal carcinoma, and their effects in an in vivo setting remain poorly known. This review discusses the relevance of endoplasmic reticulum stress activation or suppression in renal cancer cell progression and the therapeutic potential of targeting this cellular process for this cancer.

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Papp, Sylvia, Xiaochu Zhang, Eva Szabo, Marek Michalak, and Michal Opas. "Expression of Endoplasmic Reticulum Chaperones in Cardiac Development." Open Cardiovascular Medicine Journal 2, no. 1 (May 21, 2008): 31–35. http://dx.doi.org/10.2174/1874192400802010031.

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To determine if cardiogenesis causes endoplasmic reticulum stress, we examined chaperone expression. Many cardiac pathologies cause activation of the fetal gene program, and we asked the reverse: could activation of the fetal gene program during development induce endoplasmic reticulum stress/chaperones? We found stress related chaperones were more abundant in embryonic compared to adult hearts, indicating endoplasmic reticulum stress during normal cardiac development. To determine the degree of stress, we investigated endoplasmic reticulum stress pathways during cardiogenesis. We detected higher levels of ATF6α, caspase 7 and 12 in adult hearts. Thus, during embryonic development, there is large protein synthetic load but there is no endoplasmic reticulum stress. In adult hearts, chaperones are less abundant but there are increased levels of ATF6α and ER stress-activated caspases. Thus, protein synthesis during embryonic development does not seem to be as intense a stress as is required for apoptosis that is found during postnatal remodelling.

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37

Dong, Yunzhou, Conrad Fernandes, Yanjun Liu, Yong Wu, Hao Wu, Megan L. Brophy, Lin Deng, et al. "Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis." Diabetes and Vascular Disease Research 14, no. 1 (October 20, 2016): 14–23. http://dx.doi.org/10.1177/1479164116666762.

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It is well established that diabetes mellitus accelerates atherosclerotic vascular disease. Endothelial injury has been proposed to be the initial event in the pathogenesis of atherosclerosis. Endothelium not only acts as a semi-selective barrier but also serves physiological and metabolic functions. Diabetes or high glucose in circulation triggers a series of intracellular responses and organ damage such as endothelial dysfunction and apoptosis. One such response is high glucose-induced chronic endoplasmic reticulum stress in the endothelium. The unfolded protein response is an acute reaction that enables cells to overcome endoplasmic reticulum stress. However, when chronically persistent, endoplasmic reticulum stress response could ultimately lead to endothelial dysfunction and atherosclerosis. Herein, we discuss the scientific advances in understanding endoplasmic reticulum stress-induced endothelial dysfunction, the pathogenesis of diabetes-accelerated atherosclerosis and endoplasmic reticulum stress as a potential target in therapies for diabetic atherosclerosis.

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38

Lucke-Wold, Brandon P., Ryan C. Turner, Aric F. Logsdon, Linda Nguyen, Julian E. Bailes, John M. Lee, Matthew J. Robson, Bennet I. Omalu, Jason D. Huber, and Charles L. Rosen. "Endoplasmic reticulum stress implicated in chronic traumatic encephalopathy." Journal of Neurosurgery 124, no. 3 (March 2016): 687–702. http://dx.doi.org/10.3171/2015.3.jns141802.

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OBJECT Chronic traumatic encephalopathy is a progressive neurodegenerative disease characterized by neurofibrillary tau tangles following repetitive neurotrauma. The underlying mechanism linking traumatic brain injury to chronic traumatic encephalopathy has not been elucidated. The authors investigate the role of endoplasmic reticulum stress as a link between acute neurotrauma and chronic neurodegeneration. METHODS The authors used pharmacological, biochemical, and behavioral tools to assess the role of endoplasmic reticulum stress in linking acute repetitive traumatic brain injury to the development of chronic neurodegeneration. Data from the authors’ clinically relevant and validated rodent blast model were compared with those obtained from postmortem human chronic traumatic encephalopathy specimens from a National Football League player and World Wrestling Entertainment wrestler. RESULTS The results demonstrated strong correlation of endoplasmic reticulum stress activation with subsequent tau hyperphosphorylation. Various endoplasmic reticulum stress markers were increased in human chronic traumatic encephalopathy specimens, and the endoplasmic reticulum stress response was associated with an increase in the tau kinase, glycogen synthase kinase–3β. Docosahexaenoic acid, an endoplasmic reticulum stress inhibitor, improved cognitive performance in the rat model 3 weeks after repetitive blast exposure. The data showed that docosahexaenoic acid administration substantially reduced tau hyperphosphorylation (t = 4.111, p < 0.05), improved cognition (t = 6.532, p < 0.001), and inhibited C/EBP homology protein activation (t = 5.631, p < 0.01). Additionally the data showed, for the first time, that endoplasmic reticulum stress is involved in the pathophysiology of chronic traumatic encephalopathy. CONCLUSIONS Docosahexaenoic acid therefore warrants further investigation as a potential therapeutic agent for the prevention of chronic traumatic encephalopathy.

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Guo, Shulong, Shaoya Wang, Youxiao Zeng, and Qiaosheng Hu. "Stress-Associated Endoplasmic Reticulum Protein 1 Protected High Glucose-Induced Islet β Cells from Apoptosis by Attenuating Endoplasmic Reticulum Stress." Journal of Biomaterials and Tissue Engineering 9, no. 12 (December 1, 2019): 1731–38. http://dx.doi.org/10.1166/jbt.2019.2192.

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The incidence of type II diabetes caused by islet cell injury is increasing in recent years. Endoplasmic reticulum stress is one of the crucial causes of islet β cell damage, and stress-associated endoplasmic reticulum protein 1 (SERP1) could inhibit the occurrence and development of endoplasmic reticulum stress. But whether SERP1 could inhibit the damage of islet β cell caused by endoplasmic reticulum stress is unclear. In this study, we detected the levels of SERP1 and endoplasmic reticulum stress related proteins (p-PERK, p-Eif2 α, ATF-4 and CHOP) by western blotting. Next the lentivirus was used to construct the islet cell line which was stable overexpressed SERP1. Then the expression of endoplasmic reticulum stress related proteins and inflammatory factors was determined with western blotting. At last the apoptosis rates of islet β cells were detected by flow cytometry. We found that high glucose medium promoted the expression of p-PERK, p-Eif2 α, ATF-4 and CHOP while downregulated the levels of SERP1 in isletβ cells. Moreover, overexpression of SERP1 induced the downregulation of levels of p-PERK, p-Eif2 α, ATF-4, CHOP, TNF-α , IL-1β and IL-6 and alleviated the apoptosis of islet cells. At last, the overexpression of CHOP rescued the apoptosis rates and the expression of TNF-α, IL-1β and IL-6. These results indicated SERP1 relieved the inflammation response and apoptosis of islet β cells by inhibiting the expression of CHOP and alleviating the endoplasmic reticulum stress induced damage.

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Liu, Xiaoqing, Riaz Hussain, Khalid Mehmood, Zhaoxin Tang, Hui Zhang, and Ying Li. "Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy." BioMed Research International 2022 (September 17, 2022): 1–12. http://dx.doi.org/10.1155/2022/6459585.

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Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen-containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial-endoplasmic reticulum communication-mediated oxidative stress and autophagy. Mitochondria and endoplasmic reticulum being important organelles in cells are directly or indirectly connected to each other through mitochondria-associated endoplasmic reticulum membranes and jointly regulate oxidative stress and autophagy. The reactive oxygen species (ROS) produced by the mitochondrial respiratory chain are the main inducers of oxidative stress. Damaged mitochondria can be effectively cleared by the process of mitophagy mediated by PINK1/parkin pathway, Nix/BNIP3 pathways, and FUNDC1 pathway, avoiding excessive ROS production. However, the mechanism of mitochondrial-endoplasmic reticulum communication in the regulation of oxidative stress and autophagy is rarely known. For this reason, this review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca2+ and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial-endoplasmic reticulum communication.

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41

Michalak, Marek, and Myung Chan Gye. "Endoplasmic reticulum stress in periimplantation embryos." Clinical and Experimental Reproductive Medicine 42, no. 1 (2015): 1. http://dx.doi.org/10.5653/cerm.2015.42.1.1.

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WANG, Ying, Ye XIONG, Yan SHANG, Qiang LI, and Chong BAI. "Endoplasmic reticulum stress and bronchial asthma." Academic Journal of Second Military Medical University 36, no. 1 (2015): 74. http://dx.doi.org/10.3724/sp.j.1008.2015.00074.

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43

Oshitari, Toshiyuki. "Endoplasmic reticulum stress and diabetic retinopathy." Vascular Health and Risk Management 4, no. 1 (2008): 115–22. http://dx.doi.org/10.2147/vhrm.2008.04.01.115.

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Oshitari, Toshiyuki. "Endoplasmic reticulum stress and diabetic retinopathy." Vascular Health and Risk Management Volume 4 (February 2008): 115–22. http://dx.doi.org/10.2147/vhrm.s2293.

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45

ARAKI, Eiichi, Seiichi OYADOMARI, and Masataka MORI. "Endoplasmic Reticulum Stress and Diabetes Mellitus." Internal Medicine 42, no. 1 (2003): 7–14. http://dx.doi.org/10.2169/internalmedicine.42.7.

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E. Duffee, Lillian, Jon L. Boatwright, Faris H. Pacha, James M. Shockley, Karolina M. Pajerowska-Mukhtar, and M. Shahid Mukhtar. "Eukaryotic Endoplasmic Reticulum Stress-Sensing Mechanisms." Advances in Life Sciences 2, no. 6 (January 7, 2013): 148–55. http://dx.doi.org/10.5923/j.als.20120206.02.

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Ghemrawi, Rose, Shyue-Fang Battaglia-Hsu, and Carole Arnold. "Endoplasmic Reticulum Stress in Metabolic Disorders." Cells 7, no. 6 (June 19, 2018): 63. http://dx.doi.org/10.3390/cells7060063.

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Duan, Qirui, Ying Zhou, and Dong Yang. "Endoplasmic reticulum stress in airway hyperresponsiveness." Biomedicine & Pharmacotherapy 149 (May 2022): 112904. http://dx.doi.org/10.1016/j.biopha.2022.112904.

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Song, Chang-Hwa. "Endoplasmic Reticulum Stress Responses and Apoptosis." Journal of Bacteriology and Virology 42, no. 3 (2012): 196. http://dx.doi.org/10.4167/jbv.2012.42.3.196.

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Zeeshan, Hafiz, Geum Lee, Hyung-Ryong Kim, and Han-Jung Chae. "Endoplasmic Reticulum Stress and Associated ROS." International Journal of Molecular Sciences 17, no. 3 (March 2, 2016): 327. http://dx.doi.org/10.3390/ijms17030327.

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