Acute ethanol exposure-induced autophagy-mediated cardiac injury via activation of the ROS-JNK-Bcl-2 pathway

2017 ◽  
Vol 233 (2) ◽  
pp. 924-935 ◽  
Author(s):  
Zhongxin Zhu ◽  
Yewei Huang ◽  
Lingchun Lv ◽  
Youli Tao ◽  
Minglong Shao ◽  
...  
Keyword(s):  
Cardiac Injury ◽  
Ethanol Exposure ◽  
Acute Ethanol

Schisandrin B Protects against Acute Ethanol-Induced Cardiac Injury by Downregulating Autophagy via the NOX4/ROS Pathway

Pharmacology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Youli Tao ◽  
Hua Zhou ◽  
Lili Huang ◽  
Xiaoyin Xu ◽  
Yun Huang ◽  
...  
Keyword(s):  
Redox Regulation ◽  
Cardiac Injury ◽  
Ethanol Exposure ◽  
Autophagic Flux ◽  
Schisandrin B ◽  
Ros Accumulation ◽  
Acute Ethanol ◽  
H9c2 Myoblasts ◽  
And Function

<b><i>Introduction:</i></b> Although oxidative stress has been demonstrated to mediate acute ethanol-induced changes in autophagy in the heart, the precise mechanism behind redox regulation in acute ethanol heart disease remains largely unknown. <b><i>Methods:</i></b> Wild-type C57BL/6 mice were intraperitoneally injected with ethanol (3 g/kg/day) for 3 consecutive days. The effects of ethanol on cultured primary cardiomyocytes and H9c2 myoblasts were also studied in vitro. Levels of autophagic flux, cardiac apoptosis and function, reactive oxygen species (ROS) accumulation, NOX4, and NOX2 were examined. The <i>NOX4</i> gene was knocked down with NOX4 siRNA. <b><i>Results:</i></b> In this study, we demonstrated that schisandrin B inhibited acute ethanol-induced autophagy and sequent apoptosis. In addition, schisandrin B treatment improved cardiac function in ethanol-treated mice. Furthermore, NOX4 protein expression was increased during acute ethanol exposure, and the upregulation of NOX4 was significantly inhibited by schisandrin B treatment. The knockdown of NOX4 prevented ROS accumulation, cell autophagy, and apoptosis. <b><i>Conclusion:</i></b> These results highlight that NOX4 is a critical mediator of ROS and elaborate the role of the NOX4/ROS axis in the effect of schisandrin B on autophagy and autophagy-mediated apoptosis in acute ethanol exposure, which suggests a therapeutic strategy for acute alcoholic cardiomyopathy.

scholarly journals Acute ethanol exposure disrupts VEGF receptor cell signaling in endothelial cells

2008 ◽  
Vol 295 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Katherine A. Radek ◽  
Elizabeth J. Kovacs ◽  
Richard L. Gallo ◽  
Luisa A. DiPietro
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Signaling ◽  
Network Formation ◽  
Ethanol Exposure ◽  
Capillary Network ◽  
Ethanol Metabolism ◽  
Vegf Receptor ◽  
Acute Ethanol

Physiological angiogenesis is regulated by various factors, including signaling through vascular endothelial growth factor (VEGF) receptors. We previously reported that a single dose of ethanol (1.4 g/kg), yielding a blood alcohol concentration of 100 mg/dl, significantly impairs angiogenesis in murine wounds, despite adequate levels of VEGF, suggesting direct effects of ethanol on endothelial cell signaling (40). To examine the mechanism by which ethanol influences angiogenesis in wounds, we employed two different in vitro angiogenesis assays to determine whether acute ethanol exposure (100 mg/dl) would have long-lasting effects on VEGF-induced capillary network formation. Ethanol exposure resulted in reduced VEGF-induced cord formation on collagen and reduced capillary network structure on Matrigel in vitro. In addition, ethanol exposure decreased expression of endothelial VEGF receptor-2, as well as VEGF receptor-2 phosphorylation in vitro. Inhibition of ethanol metabolism by 4-methylpyrazole partially abrogated the effect of ethanol on endothelial cell cord formation. However, mice treated with t-butanol, an alcohol not metabolized by alcohol dehydrogenase, exhibited no change in wound vascularity. These results suggest that products of ethanol metabolism are important factors in the development of ethanol-induced changes in endothelial cell responsiveness to VEGF. In vivo, ethanol exposure caused both decreased angiogenesis and increased hypoxia in wounds. Moreover, in vitro experiments demonstrated a direct effect of ethanol on the response to hypoxia in endothelial cells, as ethanol diminished nuclear hypoxia-inducible factor-1α protein levels. Together, the data establish that acute ethanol exposure significantly impairs angiogenesis and suggest that this effect is mediated by changes in endothelial cell responsiveness to both VEGF and hypoxia.

scholarly journals Induction of autophagy by zinc during acute ethanol exposure (122.1)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Juan Liuzzi ◽  
Lorenzo Menzel ◽  
Changwon Yoo
Keyword(s):  
Ethanol Exposure ◽  
Acute Ethanol

scholarly journals Acute ethanol stress induces sumoylation of conserved chromatin structural proteins in Saccharomyces cerevisiae

2021 ◽  
pp. mbc.E20-11-0715
Author(s):  
Amanda I. Bradley ◽  
Nicole M. Marsh ◽  
Heather R. Borror ◽  
Kaitlyn E. Mostoller ◽  
Amber I. Gama ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ethanol Exposure ◽  
S Phase ◽  
Structural Proteins ◽  
Ethanol Stress ◽  
Post Translational Modification ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cycle Arrest ◽  
Chromatin Structural ◽  
Acute Ethanol

Stress is ubiquitous to life and can irreparably damage essential biomolecules and organelles in cells. To survive, organisms must sense and adapt to stressful conditions. One highly conserved adaptive stress response is through the post-translational modification of proteins by the small ubiquitin-like modifier (SUMO). Here, we examine the effects of acute ethanol stress on protein sumoylation in the budding yeast Saccharomyces cerevisiae . We found that cells exhibit a transient sumoylation response after acute exposure to ≤ 7.5% ethanol. By contrast, the sumoylation response becomes chronic at 10% ethanol exposure. Mass spectrometry analyses identified 18 proteins that are sumoylated after acute ethanol exposure, with 15 known to associate with chromatin. Upon further analysis, we found that the chromatin structural proteins Smc5 and Smc6 undergo ethanol-induced sumoylation that depends on the activity of the E3 SUMO ligase Mms21. Using cell-cycle arrest assays, we observed that Smc5 and Smc6 ethanol-induced sumoylation occurs during G1 and G2/M phases but not S phase. Acute ethanol exposure also resulted in the formation of Rad52 foci at levels comparable to Rad52 foci formation after exposure to the DNA alkylating agent methyl methanesulfonate (MMS). MMS exposure is known to induce the intra-S phase DNA damage checkpoint via Rad53 phosphorylation, but ethanol exposure did not induce Rad53 phosphorylation. Ethanol abrogated the effect of MMS on Rad53 phosphorylation when added simultaneously. From these studies, we propose that acute ethanol exposure induces a change in chromatin leading to sumoylation of specific chromatin-structural proteins.

scholarly journals Acute ethanol exposure inhibits macrophage IL-6 production: role of p38 and ERK1/2 MAPK

2003 ◽  
Vol 75 (3) ◽  
pp. 553-559 ◽  
Author(s):  
Joanna Goral ◽  
Mashkoor A. Choudhry ◽  
Elizabeth J. Kovacs
Keyword(s):  
Ethanol Exposure ◽  
Acute Ethanol

Effects of Acute Ethanol Exposure on the Early Inflammatory Response After Excisional Injury

2007 ◽  
Vol 31 (2) ◽  
pp. 317-323 ◽  
Author(s):  
Daniel J. Fitzgerald ◽  
Katherine A. Radek ◽  
Mitchell Chaar ◽  
Douglas E. Faunce ◽  
Luisa A. DiPietro ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Ethanol Exposure ◽  
Acute Ethanol ◽  
Early Inflammatory Response
Sign in / Sign up

Export Citation Format

Share Document