scholarly journals PI3‐kinase/Akt pathway‐regulated membrane transportation of acid‐sensing ion channel 1a/Calcium ion influx/endoplasmic reticulum stress activation on PDGF‐induced HSC Activation

2019 ◽  
Vol 23 (6) ◽  
pp. 3940-3950 ◽  
Author(s):  
Longquan Zuo ◽  
Yueqin Zhu ◽  
Lili Hu ◽  
Yanyi Liu ◽  
Yinghong Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Ion Channel ◽  
Calcium Ion ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Ion Influx ◽  
Stress Activation

scholarly journals High Doses of Dexamethasone Induce Endoplasmic Reticulum Stress-Mediated Apoptosis by Promoting Calcium Ion Influx-Dependent CHOP Expression in Osteoblasts

2021 ◽  
Author(s):  
Yunshan Guo ◽  
Dingjun Hao
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
Calcium Ion ◽  
Caspase 3 ◽  
Combined Treatment ◽  
Caspase 12 ◽  
Ion Influx ◽  
High Doses ◽  
In Cells

Abstract Background: The molecular mechanisms by which dexamethasone (Dex) induces apoptosis in osteoblasts remain unclear.Materials and Methods: MC3T3-E1 cells were treated with 0, 10-8, 10-6, and 10-4 M Dex for 24 h. The expression of ATF6, and phosphorylated PERK and IRE1, cell apoptosis, and the activity of caspase-12 and caspase-3 were measured. The expression of CHOP and the rate of influx of calcium ions were also measured in cells treated with 0 and 10-4 M Dex for 24 h. The effect of 2-APB treatment was assessed in cells treated with 0 or 10-4 M Dex.Results: The levels of ATF6 and phosphorylated PERK and IRE1 increased in a dose-dependent manner in MC3T3-E1 cells treated with 10-8, 10-6, and 10-4 M Dex, compared to in cells treated with 0 M Dex (P <0.05). Cells treated with 10-6 and 10-4 M Dex had significantly increased cell apoptosis rates and caspase-12 and caspase-3 activity compared to the control (P <0.05). Cells treated with 10-4 M Dex had significantly increased levels of CHOP and calcium ion influx rates compared to in the control (P <0.05). Combined treatment with 10-4 M Dex and 2-APB abrogated the observed increases in cell apoptosis and the activity of caspase-12 and caspase-3 (P>0.05). Conclusion: High doses of Dex induce endoplasmic reticulum stress-mediated apoptosis by promoting calcium ion influx-dependent expression of CHOP, and the activation of caspase-12 and caspase-3 in osteoblasts. Combined treatment with 2-APB protects the cells from the effects of Dex, preventing endoplasmic reticulum stress-mediated apoptosis.

scholarly journals High doses of dexamethasone induce endoplasmic reticulum stress-mediated apoptosis by promoting calcium ion influx-dependent CHOP expression in osteoblasts

2021 ◽  
Author(s):  
Yunshan Guo ◽  
Dingjun Hao ◽  
Huimin Hu
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
Calcium Ion ◽  
Caspase 3 ◽  
Chop Expression ◽  
Induce Endoplasmic Reticulum Stress ◽  
Caspase 12 ◽  
Ion Influx ◽  
High Doses

Abstract Background The long-term use of dexamethasone (Dex), a well-known immunosuppressant, leads to an imbalance in bone metabolism and rapid decline of bone mineral density due to apoptosis of osteoblasts. The molecular mechanisms by which Dex induces osteoblast apoptosis remain unclear. Materials and methods MC3T3-E1 cells were treated with 0, 10−8, 10−6, and 10−4 M Dex for 24 h. ATF6, phosphorylated PERK, PERK, phosphorylated IRE1, and IRE1 expression, cell apoptosis, and caspase-12 and caspase-3 activity were measured. CHOP expression and calcium ion influx rate were measured in cells treated with 0 and 10−4 M Dex for 24 h. The effect of 2-APB treatment was assessed in cells treated with 0 or 10−4 M Dex. Results Levels of ATF6 and phosphorylated PERK and IRE1 increased in a dose-dependent manner in MC3T3-E1 cells treated with 10−8, 10−6, and 10−4 M Dex, compared to the control group (P < 0.05). Cells treated with 10−6 and 10−4 M Dex had significantly increased apoptotic rates and caspase-12 and caspase-3 activities (P < 0.05). Cells treated with 10−4 M Dex had significantly increased CHOP levels and calcium ion influx rates (P < 0.05). Combined treatment with 10−4 M Dex and 2-APB abrogated the observed increases in cell apoptosis and caspase-12 and caspase-3 activities (P < 0.05). Conclusions High doses of Dex induce CHOP expression by promoting calcium ion influx-dependent induction of ATF6, phosphorylated PERK and phosphorylated IRE1, which induce endoplasmic reticulum stress-mediated apoptosis in osteoblasts. 2-APB protects the osteoblasts from the effects of Dex, preventing endoplasmic reticulum stress-mediated apoptosis.

scholarly journals PI3-kinase/Akt Pathway-Regulated Membrane Insertion of Acid-Sensing Ion Channel 1a Underlies BDNF-Induced Pain Hypersensitivity

2012 ◽  
Vol 32 (18) ◽  
pp. 6351-6363 ◽  
Author(s):  
B. Duan ◽  
D.-S. Liu ◽  
Y. Huang ◽  
W.-Z. Zeng ◽  
X. Wang ◽  
...  
Keyword(s):  
Ion Channel ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Membrane Insertion ◽  
Pain Hypersensitivity

Bufotalin-induced apoptosis in osteoblastoma cells is associated with endoplasmic reticulum stress activation

2014 ◽  
Vol 451 (1) ◽  
pp. 112-118 ◽  
Author(s):  
Yun-Rong Zhu ◽  
Yong Xu ◽  
Jian-Feng Fang ◽  
Feng Zhou ◽  
Xiong-Wei Deng ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Induced Apoptosis ◽  
Stress Activation

Saturated lipids decrease mitofusin 2 leading to endoplasmic reticulum stress activation and insulin resistance in hypothalamic cells

2015 ◽  
Vol 1627 ◽  
pp. 80-89 ◽  
Author(s):  
Brenda Diaz ◽  
Lizeth Fuentes-Mera ◽  
Armando Tovar ◽  
Teresa Montiel ◽  
Lourdes Massieu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitofusin 2 ◽  
Hypothalamic Cells ◽  
Stress Activation
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