Intraneuronal amyloid β oligomers cause cell death via endoplasmic reticulum stress, endosomal/lysosomal leakage, and mitochondrial dysfunction in vivo

2011 ◽  
Vol 89 (7) ◽  
pp. 1031-1042 ◽  
Author(s):  
Tomohiro Umeda ◽  
Takami Tomiyama ◽  
Naomi Sakama ◽  
Saya Tanaka ◽  
Mary P. Lambert ◽  
...  
RSC Advances ◽  
2019 ◽  
Vol 9 (71) ◽  
pp. 41639-41648 ◽  
Author(s):  
Farazul Haque ◽  
Nitish Kumar Verma ◽  
Mohammad Alfatah ◽  
Swati Bijlani ◽  
Mani Shankar Bhattacharyya

Sophorolipid induces ROS generation in C. albicans leading to mitochondrial dysfunction and ER stress followed by the release of Ca2+ ions (from the ER lumen) that enter mitochondria and further magnify ROS generation leading to cell death.


2016 ◽  
Vol 20 (9) ◽  
pp. 1749-1760 ◽  
Author(s):  
Chi-Ming Chan ◽  
Duen-Yi Huang ◽  
Yi-Pin Huang ◽  
Shu-Hao Hsu ◽  
Lan-Ya Kang ◽  
...  

2017 ◽  
Vol 13 (4) ◽  
pp. 379-390 ◽  
Author(s):  
Gina Hadley ◽  
Ain A Neuhaus ◽  
Yvonne Couch ◽  
Daniel J Beard ◽  
Bryan A Adriaanse ◽  
...  

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.


2012 ◽  
Vol 209 (3) ◽  
pp. 203-210 ◽  
Author(s):  
Chuen-Lin Huang ◽  
Yi-Chao Lee ◽  
Ying-Chen Yang ◽  
Tsun-Yung Kuo ◽  
Nai-Kuei Huang

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