SA4503, a sigma-1 receptor agonist, prevents cultured cortical neurons from oxidative stress-induced cell death via suppression of MAPK pathway activation and glutamate receptor expression

2010 ◽  
Vol 469 (3) ◽  
pp. 303-308 ◽  
Author(s):  
Tuerhong Tuerxun ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Emi Kumamaru ◽  
Hiromi Kitazawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cortical Neurons ◽  
Receptor Agonist ◽  
Mapk Pathway ◽  
Receptor Expression ◽  
Sigma 1 Receptor ◽  
Pathway Activation ◽  
Sigma 1 ◽  
Cultured Cortical Neurons

Effect of a sigma-1 receptor agonist, cutamesine dihydrochloride (SA4503), on photoreceptor cell death against light-induced damage

2015 ◽  
Vol 132 ◽  
pp. 64-72 ◽  
Author(s):  
Masamitsu Shimazawa ◽  
Sou Sugitani ◽  
Yuki Inoue ◽  
Kazuhiro Tsuruma ◽  
Hideaki Hara
Keyword(s):  
Cell Death ◽  
Receptor Agonist ◽  
Photoreceptor Cell ◽  
Sigma 1 Receptor ◽  
Sigma 1

scholarly journals SA4503, A Potent Sigma-1 Receptor Ligand, Ameliorates Synaptic Abnormalities and Cognitive Dysfunction in a Mouse Model of ATR-X Syndrome

2018 ◽  
Vol 19 (9) ◽  
pp. 2811 ◽  
Author(s):  
Kouya Yamaguchi ◽  
Norifumi Shioda ◽  
Yasushi Yabuki ◽  
Chen Zhang ◽  
Feng Han ◽  
...  
Keyword(s):  
Intellectual Disability ◽  
Dendritic Spine ◽  
Cortical Neurons ◽  
Exon 2 ◽  
Sigma 1 Receptor ◽  
Axonal Development ◽  
Sigma 1 ◽  
Cultured Cortical Neurons ◽  
Model Mouse ◽  
Spine Abnormalities

α-thalassemia X-linked intellectual disability (ATR-X) syndrome is caused by mutations in ATRX. An ATR-X model mouse lacking Atrx exon 2 displays phenotypes that resemble symptoms in the human intellectual disability: cognitive defects and abnormal dendritic spine formation. We herein target activation of sigma-1 receptor (Sig-1R) that can induce potent neuroprotective and neuroregenerative effects by promoting the activity of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF). We demonstrated that treatment with SA4503, a potent activator of Sig-1R, reverses axonal development and dendritic spine abnormalities in cultured cortical neurons from ATR-X model mice. Moreover, the SA4503 treatment rescued cognitive deficits exhibited by the ATR-X model mice. We further found that significant decreases in the BDNF-protein level in the medial prefrontal cortex of ATR-X model mice were recovered with treatment of SA4503. These results indicate that the rescue of dendritic spine abnormalities through the activation of Sig-1R has a potential for post-diagnostic therapy in ATR-X syndrome.

scholarly journals Cocaine-Mediated Autophagy in Astrocytes Involves Sigma 1 Receptor, PI3K, mTOR, Atg5/7, Beclin-1 and Induces Type II Programed Cell Death

2015 ◽  
Vol 53 (7) ◽  
pp. 4417-4430 ◽  
Author(s):  
Lu Cao ◽  
Mary P. Walker ◽  
Naveen K. Vaidya ◽  
Mingui Fu ◽  
Santosh Kumar ◽  
...  
Keyword(s):  
Cell Death ◽  
Beclin 1 ◽  
Type Ii ◽  
Sigma 1 Receptor ◽  
Sigma 1 ◽  
Programed Cell Death

scholarly journals Cardioprotective Effect of the Selective Sigma-1 Receptor Agonist, SA4503

2014 ◽  
Vol 134 (6) ◽  
pp. 707-713 ◽  
Author(s):  
Kohga Hirano ◽  
Hideaki Tagashira ◽  
Kohji Fukunaga
Keyword(s):  
Receptor Agonist ◽  
Cardioprotective Effect ◽  
Sigma 1 Receptor ◽  
Sigma 1

scholarly journals Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1011-1022 ◽  
Author(s):  
T.L. Gumienny ◽  
E. Lambie ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
M.O. Hengartner
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Mapk Pathway ◽  
Apoptotic Cell ◽  
C Elegans ◽  
Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

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