ArticleCytotechnology2012
H(2)O (2)-induced secretion of tumor necrosis factor-α evokes apoptosis of cardiac myocytes through reactive oxygen species-dependent activation of p38 MAPK.
Article in Cytotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Effect and mechanism of Dichloroacetate in the treatment of stroke and the resolution strategy for side effect.European journal of medical research · 2025Review
- Myoglobin Protects Breast Cancer Cells Due to Its ROS and NO Scavenging Properties.Frontiers in endocrinology · 2021Article
- The mitochondrial ubiquitin ligase plays an anti-apoptotic role in cardiomyocytes by regulating mitochondrial fission.Journal of cellular and molecular medicine · 2016Article
- β₁-adrenoceptor stimulation promotes LPS-induced cardiomyocyte apoptosis through activating PKA and enhancing CaMKII and IκBα phosphorylation.Critical care (London, England) · 2015Article
- Testicular disorders induced by plant growth regulators: cellular protection with proanthocyanidins grape seeds extract.Cytotechnology · 2013Article
- Effect of gibberellic acid on the quality of sperm and in vitro fertilization outcome in adult male rats.Veterinary research forum : an international quarterly journal · 2013Article
- Group VIB Phospholipase A(2) promotes proliferation of INS-1 insulinoma cells and attenuates lipid peroxidation and apoptosis induced by inflammatory cytokines and oxidant agents.Oxidative medicine and cellular longevity · 2012Article
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Authors and funding
5 authors.
Funding
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Abstract
P38 mitogen-activated protein kinases (p38 MAPK) and tumor necrosis factor-α (TNF-α) play important roles in oxidative stress-induced apoptosis in cardiac myocytes. However, the regulation and functional role of cross-talk between p38 MAPK and TNF-α pathways have not yet been fully characterized in cardiac myocytes. In this study, we found that inhibition of p38 MAPK with SB-203580 (SB) reduced H(2)O(2)-stimulated secretion of TNF-α, whereas pre-activation of p38 MAPK with sodium arsenite (SA) enhanced H(2)O(2)-stimulated secretion of TNF-α. In addition, pretreatment of cells with TNF-α increased basal and H(2)O(2)-stimulated p38 MAPK and apoptosis of cardiac myocytes, and p38 MAPK-associated apoptosis of cardiac myocytes induced by TNF-α was blocked by inhibition of p38 MAPK with SB. Finally, H(2)O(2)-induced apoptosis was attenuated by the inhibitors of p38 MAPK or reactive oxygen species (ROS), whereas it was enhanced by p38 MAPK agonist SA. These results suggest that H(2)O(2)-induced secretion of TNF-α increases apoptosis of cardiac myocytes through ROS-dependent activation of p38 MAPK. This may represent a novel mechanism that TNF-α partly interplays with p38 MAPK pathways during oxidative stress-modulated apoptosis in cardiac myocytes.
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Registered trials
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