Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis

Rajamani, Uthra; Essop, M. Faadiel

doi:10.1152/ajpcell.00020.2010

Cited by 80 publications

(82 citation statements)

References 30 publications

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“…[37][38][39] The results in our study, similar to the previous reports, found that Akt-knockout liver cancer cells displayed lower p-Bad expression and higher Bad expression, cutting down Bcl-xL expression and promoting the downstreaming signals, such as cytochrome c, Apaf-1, caspase-9, and caspase-3 expression, subsequently contributing to apoptosis in cancer cells ( Figures 5A-E and 7). And Western blot and RT-PCR analysis further certify the results that Akt −/− enhanced Bad expression.…”

supporting

confidence: 91%

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Tang¹,

Tang²,

Wang³

et al. 2016

IJN

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supporting

confidence: 91%

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Tang¹,

Tang²,

Wang³

et al. 2016

IJN

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“…4). It has been observed that ROS may increase flux through the hexosamine biosynthetic pathway, resulting in greater O-GlcNacylation of proteins (101,160).…”

Section: O-linked Glycosylation (O-glcnacylation)mentioning

confidence: 99%

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Pagliaro

Moro

Tullio

et al. 2011

Antioxidants & Redox Signaling

114

152

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Post-ischemic reperfusion may result in reactive oxygen species (ROS) generation, reduced availability of nitric oxide (NO ), Ca 2+ overload, prolonged opening of mitochondrial permeability transition pore, and other processes contributing to cell death, myocardial infarction, stunning, and arrhythmias. With the discovery of the preconditioning and postconditioning phenomena, reperfusion injury has been appreciated as a reality from which protection is feasible, especially with postconditioning, which is under the control of physicians. Potentially cooperative protective signaling cascades are recruited by both pre-and postconditioning. In these pathways, phosphorylative= dephosphorylative processes are widely represented. However, cardioprotective modalities of signal transduction also include redox signaling by ROS, S-nitrosylation by NO and derivative, S-sulfhydration by hydrogen sulfide, and O-linked glycosylation with beta-N-acetylglucosamine. All these modalities can interact and regulate an entire pathway, thus influencing each other. For instance, enzymes can be phosphorylated and=or nitrosylated in specific and=or different site(s) with consequent increase or decrease of their specific activity. The cardioprotective signaling pathways are thought to converge on mitochondria, and various mitochondrial proteins have been identified as targets of these post-transitional modifications in both pre-and postconditioning. Antioxid. Redox Signal. 14, 833-850.

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“…A large number of animal experiments and clinical trials indicate that hyperglycemia enhances cardiac production of inFammatory cytokines such as interleukin (IL)-6, tumor necrosis factor (TNF)-a, and free radicals such as reactive oxygen species (ROS). These cytokines and free radicals impair cardiac contractile function, and promote the development of myocardial apoptosis, cardiac hypertrophy, and heart failure (Drimal et al 2008;Rajamani and Essop 2010). Although multiple factors contribute to high glucoseinduced cardiac damage, such as inflammatory cytokines, ROS , apoptosis , and activation of several signaling pathways, including mitogen-activated protein kinase (MAPK) ) and PI3K/Akt (Cao et al 2011), the roles of NF-kB and IL-1b in high glucose-induced inflammation and cardiac insults have attracted attention.…”

Section: Introductionmentioning

confidence: 99%

Protection of SAL B with H9C2 cells

Sun

Zuo

et al. 2015

Pharmaceutical Biology

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Context: Salvianolic acid B (Sal B) is regarded as a potent antidiabetic agent and has been reported to possess cardioprotective effect in vivo. Objective: This study investigated the cardioprotective effects of Sal B on H9c2 cells injury caused by high glucose in vitro, and clarified the possible mechanisms. Materials and methods: Di ferent concentrations of Sal B were incubated with cells for 12 h prior being exposed to high glucose for 24 h. Cardioprotective effects of Sal B were evaluated using CCK-8 assay, ELISA, Hoechst 33258 nucleus staining, and western blot. Results: Following a 24 h exposure of H9c2 to high glucose, obvious reduction was found in cell viability (45%), GSH (54.8 ± 9.4 ng/mg protein), catalase (1.22 ± 0.12 U/mg protein), and GPX level (67.9 ± 9.4 U/mg protein), which were associated with the increases of GSSG (1.99 ± 0.28 ng/mg protein) and ROS (2.00 ± 0.19 RFU/mg protein) production. High glucose also elevated IL-6 (1.8-fold), IL-1b (1.9-fold), and TNF-a (1.6-fold) level, as well as induced cell apoptosis and NF-kB (6.1-fold) activation. However, Sal B (25 and 50 mM) elevated cell viability (28% and 44%), ameliorated oxidative stress (GSH, 1.3-and 1.6-fold; catalase, 1.9-and 2.0-fold; GPX, 1.1-and 1.4-fold; GSSG, 0.9-and 0.8-fold; ROS, 0.6-and 0.5-fold), and inflammatory response (IL-6, 0.9-and 0.7-fold; IL-1b, 0.8-and 0.6-fold; TNF-a, 0.9-and 0.8-fold), and inhibited cell apoptosis and NF-kB (0.5-and 0.2-fold) expression. Conclusion: Sal B attenuated high glucose-induced injury and cytotoxicity through inhibiting inflammatory cytokine production in H9c2 cardiac cells. ARTICLE HISTORY

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Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis

Abstract: Rajamani U, Essop MF. Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis.

Cited by 80 publications

References 30 publications

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Protection of SAL B with H9C2 cells

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Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis

Abstract: Rajamani U, Essop MF. Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis.

Cited by 80 publications

References 30 publications

Upregulation of Akt/NF-&kappa;B-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Upregulation of Akt/NF-&kappa;B-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Protection of SAL B with H9C2 cells

Contact Info

Product

Resources

About

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle