scholarly journals Vibrio vulnificus VvhA induces autophagy-related cell death through the lipid raft-dependent c-Src/NOX signaling pathway

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Eun Ju Song ◽  
Sei-Jung Lee ◽  
Hyeon Su Lim ◽  
Jun Sung Kim ◽  
Kyung Ku Jang ◽  
...  
Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 631 ◽  
Author(s):  
Ji-Yun Kim ◽  
Young-Min Lee ◽  
Do-Wan Kim ◽  
Taesun Min ◽  
Sei-Jung Lee

Curcumin, a hydrophobic polyphenol of turmeric, has a variety of biological functions as a herbal supplement, but its poor gastric absorption rate is one of the major factors limiting its oral bioavailability. In the present study, we have investigated the functional role of a nanosphere loaded with curcumin (CN) during host cell death elicited by the Gram-negative bacterium V. vulnificus in human gastrointestinal epithelial HT-29 cells and an ileal-ligated mouse model. The recombinant protein (r) VvhA produced by V. vulnificus significantly reduced the viability of HT-29 cells. The cytotoxic effect of rVvhA was restored upon a treatment with CN (100 ng/mL), which had shown 1000-fold higher anti-apoptotic efficacy than curcumin. CN inhibited the phosphorylation of c-Src and PKC mediated by intracellular ROS responsible for the distinctive activation of the MAPKs in rVvhA-treated HT-29 cells. Interestingly, CN significantly restored the expression of Bax, Bcl-2, and cleaved caspase-3 as regulated by the phosphorylation of NF-κB. In mouse models of V. vulnificus infection, treatment with CN had a blocking effect that elevated the levels of TUNEL-positive DNA fragmentation and apoptosis-related proteins. These results indicate that CN is a functional agent that manipulates the V. vulnificus VvhA signaling pathway responsible for gastrointestinal cell death.


2016 ◽  
Vol 54 (12) ◽  
pp. 1343-1404
Author(s):  
G Metzger ◽  
P Di Fazio ◽  
DK Bartsch ◽  
T Gress ◽  
TT Wissniowski

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Lan Jin ◽  
Yunhe Chen ◽  
Dan Cheng ◽  
Zhikai He ◽  
Xinyi Shi ◽  
...  

AbstractColorectal cancer (CRC) is one of the most aggressive and lethal cancers. The role of autophagy in the pathobiology of CRC is intricate, with opposing functions manifested in different cellular contexts. The Yes-associated protein (YAP), a transcriptional coactivator inactivated by the Hippo tumor-suppressor pathway, functions as an oncoprotein in a variety of cancers. In this study, we found that YAP could negatively regulate autophagy in CRC cells, and consequently, promote tumor progression of CRC in vitro and in vivo. Mechanistically, YAP interacts with TEAD forming a complex to upregulate the transcription of the apoptosis-inhibitory protein Bcl-2, which may subsequently facilitate cell survival by suppressing autophagy-related cell death; silencing Bcl-2 expression could alleviate YAP-induced autophagy inhibition without affecting YAP expression. Collectively, our data provide evidence for YAP/Bcl-2 as a potential therapeutic target for drug exploration against CRC.


2020 ◽  
Vol 168 (1) ◽  
pp. 1-6
Author(s):  
Chikashi Yoshimura ◽  
Akiomi Nagasaka ◽  
Hitoshi Kurose ◽  
Michio Nakaya

Abstract Myocardial infarction is one of the major causes of death worldwide. Many heart cells die during myocardial infarction through various processes such as necrosis, apoptosis, necroptosis, autophagy-related cell death, pyroptosis and ferroptosis. These dead cells in infarcted hearts expose the so-called ‘eat-me’ signals, such as phosphatidylserine, on their surfaces, enhancing their removal by professional and non-professional phagocytes. Clearance of dead cells by phagocytes in the diseased hearts plays a crucial role in the pathology of myocardial infarction by inhibiting the inflammatory responses caused by the leakage of contents from dead cells. This review focuses on the rapidly growing understanding of the molecular mechanisms of dead cell phagocytosis, termed efferocytosis, during myocardial infarction, which contributes to the pathophysiology of myocardial infarction.


2012 ◽  
Vol 61 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Haiyan Lou ◽  
Xu Jing ◽  
Dongmei Ren ◽  
Xinbing Wei ◽  
Xiumei Zhang

1997 ◽  
Vol 8 (8) ◽  
pp. 611-613 ◽  
Author(s):  
Jamal Nasir ◽  
Jane L. Theilmann ◽  
John P. Vaillancourt ◽  
Neil A. Munday ◽  
Ambereen Ali ◽  
...  

2013 ◽  
Vol 117 (26) ◽  
pp. 7929-7940 ◽  
Author(s):  
Bruno M. Castro ◽  
Aleksander Fedorov ◽  
Valentin Hornillos ◽  
Javier Delgado ◽  
A Ulises Acuña ◽  
...  

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