Camellia euphlebia protects against corticosterone-induced apoptosis in differentiated PC12 cells by regulating the mitochondrial apoptotic pathway and PKA/CREB/BDNF signaling pathway

2019 ◽  
Vol 126 ◽  
pp. 211-222 ◽  
Author(s):  
Dongye He ◽  
Ning Wang ◽  
Xuan Sai ◽  
Xiaoyu Li ◽  
Yongping Xu
Keyword(s):  
Signaling Pathway ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Bdnf Signaling ◽  
Induced Apoptosis ◽  
Camellia Euphlebia

MicroRNA-15b enhances hypoxia/reoxygenation-induced apoptosis of cardiomyocytes via a mitochondrial apoptotic pathway

APOPTOSIS ◽  
2013 ◽  
Vol 19 (1) ◽  
pp. 19-29 ◽  
Author(s):  
Lifeng Liu ◽  
Guoming Zhang ◽  
Zhuo Liang ◽  
Xiuhua Liu ◽  
Tiande Li ◽  
...  
Keyword(s):  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Induced Apoptosis ◽  
Hypoxia Reoxygenation

scholarly journals Enterovirus 71 2B Induces Cell Apoptosis by Directly Inducing the Conformational Activation of the Proapoptotic Protein Bax

2016 ◽  
Vol 90 (21) ◽  
pp. 9862-9877 ◽  
Author(s):  
Haolong Cong ◽  
Ning Du ◽  
Yang Yang ◽  
Lei Song ◽  
Wenliang Zhang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Enterovirus 71 ◽  
Terminal Region ◽  
Ev71 Infection ◽  
Apoptotic Pathway ◽  
Hydrophobic Region ◽  
Mitochondrial Apoptotic Pathway ◽  
Proapoptotic Protein ◽  
2B Protein ◽  
Induced Apoptosis

ABSTRACTTo survive and replicate within a host, many viruses have evolved strategies that target crucial components within the apoptotic cascade, leading to either inhibition or induction of cell apoptosis. Enterovirus 71 (EV71) infections have been demonstrated to impact the mitochondrial apoptotic pathway and induce apoptosis in many cell lines. However, the detailed mechanism of EV71-induced apoptosis remains to be elucidated. In this study, we report that EV71 2B protein (2B) localized to the mitochondria and induced cell apoptosis by interacting directly with and activating the proapoptotic protein Bax. 2B recruited Bax to the mitochondria and induced Bax conformational activation. In addition, mitochondria isolated from 2B-expressing cells that were treated with a recombinant Bax showed increased Bax interaction and cytochromec(Cytc) release. Importantly, apoptosis in cells with either EV71 infection or 2B expression was dramatically reduced in Bax knockdown cells but not in Bak knockdown cells, suggesting that Bax played a pivotal role in EV71- or 2B-induced apoptosis. Further studies indicate that a hydrophobic region of 18 amino acids (aa) in the C-terminal region of 2B (aa 63 to 80) was responsible for the location of 2B in the mitochondria. A hydrophilic region of 14 aa in the N-terminal region of 2B was functional in Bax interaction and its subsequent activation. Moreover, overexpression of the antiapoptotic protein Bcl-XLabrogates 2B-induced release of Cytcand caspase activation. Therefore, this study provides direct evidence that EV71 2B induces cell apoptosis and impacts the mitochondrial apoptotic pathway by directly modulating the redistribution and activation of proapoptotic protein Bax.IMPORTANCEEV71 infections are usually accompanied by severe neurological complications. It has also been postulated that the induction of cell apoptosis resulting from tissue damage is a possible process of EV71-related pathogenesis. In this study, we report that EV71 2B protein (2B) localized to the mitochondria and induced cell apoptosis by interacting directly with and activating the proapoptotic protein Bax. This study provides evidence that EV71 induces cell apoptosis by modulating Bax activation and reveals important clues regarding the mechanism of Cytcrelease and mitochondrial permeabilization during EV71 infection.

scholarly journals Pharmacological and Molecular Evidence of Neuroprotective Curcumin Effects Against Biochemical and Behavioral Sequels Caused by Methamphetamine: Possible Function of CREB-BDNF Signaling Pathway

2021 ◽  
Author(s):  
Mina Gholami ◽  
◽  
Farzad Hozuri ◽  
Setayesh Abdolkarimi ◽  
Mahsa Mahmoudi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Interleukin 1 ◽  
Male Rats ◽  
Molecular Evidence ◽  
Necrosis Factor Alpha ◽  
Multiple Parameters ◽  
Pathway Activation ◽  
Factor Alpha ◽  
Bdnf Signaling ◽  
Induced Apoptosis

The neuroprotective impact of curcumin and the role of CREB-BDNF signaling in this way was evaluated in methamphetamine (METH)-induced neurodegeneration in rats. Sixty adult male rats were randomly split into 6 groups. While normal saline and 10 mg / kg METH were administered intraperitoneally in Groups 1 and 2, Groups 3, 4, 5 and 6 received METH (10 mg/kg) and Curcumin (10, 20, 40 and 80 mg/kg respectively) simultaneously. Morris Water Maze (MWM), oxidative hippocampal, antioxidant, inflammatory, apoptotic, and CREB and BDNF were assessed. We've found that METH disturbs learning and memory. Concurrent curcumin therapy (40 and 80 mg / kg) decreased cognitive disturbance caused by METH. Multiple parameters, such as lipid peroxidation, oxidized form of glutathione (GSSG), interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and Bax, increased by METH therapy, although the reduced type of glutathione (GSH), Bcl-2, P-CREB and BDNF concentrations in the hippocampus decreased. Different doses of curcumin adversely attenuated METH-induced apoptosis, oxidative stress and inflammation, but enhanced concentrations of P-CREB and BDNF. Curcumin-caused neuroprotection against METH-induced neurodegeneration is conducted by P-CREB / BDNF signaling pathway activation.

scholarly journals A novel endoplasmic stress mediator, Kelch domain containing 7B (KLHDC7B), increased Harakiri (HRK) in the SubAB-induced apoptosis signaling pathway

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Kinnosuke Yahiro ◽  
Kohei Ogura ◽  
Hiroyasu Tsutsuki ◽  
Sunao Iyoda ◽  
Makoto Ohnishi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Signaling Pathway ◽  
Gastrointestinal Symptoms ◽  
Parp Cleavage ◽  
Rna Seq ◽  
Gene Encoding ◽  
Apoptotic Pathway ◽  
Kelch Domain ◽  
Induced Apoptosis

AbstractLocus for Enterocyte Effacement (LEE)-positive Shiga-toxigenic Escherichia coli (STEC) contributes to many global foodborne diseases, with infection characterized by severe gastrointestinal symptoms, including bloody diarrhea. The incidence of LEE-negative STEC-mediated disease is also increasing globally. Subtilase cytotoxin (SubAB) is released by some LEE-negative STEC strains. It cleaves BiP, which is a chaperone protein located in the endoplasmic reticulum (ER), thereby causing apoptosis induced by ER stress. To date, the apoptotic signaling pathway mediated by SubAB has not been identified. In the current study, RNA-seq analysis showed that SubAB significantly induced the expression of Kelch domain containing 7B (KLHDC7B). We explored the role of KLHDC7B in the SubAB-induced apoptotic pathway. SubAB-induced KLHDC7B mRNA expression was increased after 12 h of incubation of toxin with HeLa cells. KLHDC7B expression was downregulated by knockdown of PKR-like endoplasmic reticulum kinase (PERK), CEBP homologous protein (CHOP), activating transcription factor 4 (ATF4), and CEBP β (CEBPB). KLHDC7B knockdown suppressed SubAB-stimulated CHOP expression, poly(ADP-ribose) polymerase (PARP) cleavage, and cytotoxicity. The over-expressed KLHDC7B was localized to the nucleus and cytosolic fractions. Next, we used RNA-seq to analyze the effect of KLHDC7B knockdown on apoptosis induced by SubAB, and found that the gene encoding for the pro-apoptotic Bcl-2 family protein, Harakiri (HRK), was upregulated in SubAB-treated control cells. However, this effect was not observed in SubAB-treated KLHDC7B-knockdown cells. Therefore, we identified the pathway through which SubAB-induced KLHDC7B regulates HRK expression, which is essential for apoptosis in toxin-mediated ER stress.

scholarly journals CRISPR/Cas9 Knockout of Bak Mediates Bax Translocation to Mitochondria in response to TNFα/CHX-induced Apoptosis

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Jingtian Zhang ◽  
Han Niu ◽  
Zhizhuang Joe Zhao ◽  
Xueqi Fu ◽  
Yuxiang Wang ◽  
...  
Keyword(s):  
Cell Line ◽  
Parp Cleavage ◽  
Caspase 8 ◽  
Caspase Activation ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Apoptotic Protein ◽  
Induced Apoptosis

TNFα/CHX-induced apoptosis is dependent on caspase-8 activation and regulated by Bcl-2. However, the specific participants and precise mechanisms underlying this apoptotic pathway are poorly understood. The proapoptotic proteins Bak and Bax—members of the Bcl-2 family—are essential for the functioning of the mitochondrial apoptotic pathway. In this study, we used the CRISPR/Cas9 system to knockout Bak in the human SH-SY5Y cell line and determined the effects of this knockout on TNFα/CHX-induced apoptosis. Our data showed that overexpression of Bcl-2 dramatically prevented TNFα/CHX-induced apoptosis, and then pro-apoptotic protein Bak was downregulated and became more resistant to TNFα/CHX-induced apoptosis, because both TNFα/CHX-induced PARP cleavage and caspase activation were blocked in BAK−/− cells or using specific siRNA, whereas Bax was dispensable in TNFα/CHX-induced apoptosis, as evidenced using specific siRNA. Bax translocated from the cytosol into the mitochondria in response to TNFα/CHX, and CRISPR/Cas9 knockout of Bak significantly decreased this translocation. These results indicate that TNFα/CHX-induced apoptosis does not occur in Bak−/− cells, suggesting that TNFα/CHX-induced apoptosis is Bak-dependent but Bax-independent.

scholarly journals The ER Stress-Mediated Mitochondrial Apoptotic Pathway and MAPKs Modulate Tachypacing-Induced Apoptosis in HL-1 Atrial Myocytes

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0117567 ◽  
Author(s):  
Jiaojiao Shi ◽  
Qi Jiang ◽  
Xiangwei Ding ◽  
Wenhua Xu ◽  
Dao W. Wang ◽  
...  
Keyword(s):  
Er Stress ◽  
Atrial Myocytes ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Induced Apoptosis
Sign in / Sign up

Export Citation Format

Share Document