Heat shock protein 70 protects against seizure-induced neuronal cell death in the hippocampus following experimental status epilepticus via inhibition of nuclear factor-κB activation-induced nitric oxide synthase II expression

Chang, Chiung Chih; Chen, Shang-Der; Lin, Tay-Jyi; Chang, Wen‐Cheng; Liou, Chia Wei; Chang, Alice Y.W.; Chan, Samuel H.H.; Chuang, Yao-Chung

doi:10.1016/j.nbd.2013.10.012

Cited by 38 publications

(68 citation statements)

References 38 publications

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“…In this study, PYC reduced the high level of NF-kB induced by Rot. Emerging evidence suggests that NF-kB is one of the transcriptional regulators of the nitric oxide synthase (or inducible NOS, iNOS) gene (Chan et al, 2004;Chang et al, 2014). Meanwhile, the activation of NF-kB is critical in the induction of iNOS (Xie et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Pycnogenol Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells Through Regulating NF-κB-iNOS Signaling Pathway

Gao

Chang

Zhou

et al. 2015

DNA and Cell Biology

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Parkinson's disease (PD) is a common neurodegenerative disorder characterized by dopaminergic neurons degeneration and oxidative damage may underlie this process. However, there are still no efficient drugs to cure the disease. Pycnogenol (PYC) isolated from the procyanidin-rich French maritime pine (Pinus maritime) bark has shown various antioxidant activities in previous studies. In this study, we explored its effect against rotenone (Rot)-induced neurotoxicity and the underlying mechanisms in PC12 cells. Using Rot-induced cell model of PD, we found that PYC treatment significantly increased cell viability and decreased cell apoptosis in Rot-treated PC12 cells in a dose-dependent manner. Furthermore, data showed that PYC markedly reduced inducible nitric oxide synthase (iNOS)-nitric oxide (NO) signaling in Rot-treated PC12 cells. Pretreatment with the iNOS-specific inhibitor significantly attenuated Rot-induced neurotoxicity. Moreover, PYC was found to be capable of reducing Rot-induced NF-κB activation. Blocking NF-κB signaling with its inhibitor mimicked the biological effect of PYC on Rot-induced iNOS and NO expression levels, as well as neurotoxicity in PC12 cells, suggesting that the NF-κB-iNOS signaling pathway was likely to participate in the PYC-mediated protective progress. Our results suggest that PYC protects against Rot-induced neurotoxicity in PC12 cells, and the mechanism may be associated with the downregulation of NF-κB-iNOS signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Pycnogenol Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells Through Regulating NF-κB-iNOS Signaling Pathway

Gao

Chang

Zhou

et al. 2015

DNA and Cell Biology

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“…On the one hand, the neuro-protective effect is likely achieved via antiapoptotic mechanisms in association with the overexpression of HSP70 (Zhao et al 2014). Indeed, following experimental status epilepticus via the suppression of IκB kinase (IKK) activity and deactivation of IκBα, HSP70 protects against apoptotic cell death induced by nuclear factor-κB (NF-κB) activation and the nitric oxide synthase (NOS) IIperoxynitrite signaling cascade in hippocampal CA3 and glial cells (Chang et al 2014). On the other hand, extracellular HSP70 can promote neuronal death by mediating the production of cytotoxic levels of tumor necrosis factor alpha, predominantly due to the Tlr4/Myd88 signaling cascade (Dvoriantchikova et al 2014).…”

Section: Changes In the Significance Of Hsp70 Levels In Inflammation mentioning

confidence: 99%

The detection and role of heat shock protein 70 in various nondisease conditions and disease conditions: a literature review

Qu¹,

Jia²,

Liu³

et al. 2015

Cell Stress and Chaperones

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As an intracellular polypeptide, heat shock protein 70 (HSP70) can be exposed on the plasma membrane and/or released into the circulation. However, the role of HSP70 in various nondisease and disease conditions remains unknown. Quantitative methods for the detection of HSP70 have been used in clinical studies, revealing that an increase in circulating HSP70 is associated with various types of exercise, elderly patients presenting with inflammation, mobile phones, inflammation, sepsis, chronic obstructive pulmonary disease, asthma, carotid intima-media thickness, glutamine-treated ill patients, mortality, diabetes mellitus, active chronic glomerulonephritis, and cancers. Circulating HSP70 decreases with age in humans and in obstructive sleep apnea, arteriosclerosis, atrial fibrillation (AF) following coronary artery bypass surgery, nonalcoholic fatty liver disease, moderate-to-severe alcoholic fatty liver disease, hepatic steatosis, and Helicobacter pylori infection. In conclusion, quantitative methods can be used to detect HSP70, particularly in determining circulating HSP70 levels, using more convenient and rapid screening methods. Studies have shown that changes in HSP70 are associated with various nondisease and disease conditions; thus, HSP70 might be a novel potential biomarker reflecting various nondisease conditions and also the severity of disease conditions. However, the reliability and accuracy, as well as the underlying mechanism, of this relationship remain poorly understood, and large-sample clinical research must be performed to verify the role.

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“…HSP72 is a pleiotropic cytoprotectant, not only in the cardiovascular system but also in other organs, facilitating intracellular folding or unfolding, transportation, and chaperoning of proteins (30). HSP72 has also been implicated in the disruption of 3 apoptotic pathways: 1) ATP-dependent (the Apoptosome pathway) (31); 2) ATP-independent (apoptosis-inducing factor pathway) (32); and 3) the NF-κB pathway (33). …”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effects of HSP72 Administration on Ischemia-Reperfusion Injury

Tanimoto

Parseghian

Nakahara

et al. 2017

Journal of the American College of Cardiology

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BACKGROUND Although early reperfusion is the most desirable intervention after ischemic myocardial insult, it may add to damage through oxidative stress. OBJECTIVES We investigated the cardioprotective effects of a single intravenous dose of heat shock protein (HSP72) coupled to a single-chain variable fragment (Fv) of monoclonal antibody 3E10 (3E10Fv) in a rabbit ischemia-reperfusion model. The Fv facilitates rapid transport of HSP72 into cells, even with intact membranes. METHODS A left coronary artery occlusion (40 min), reperfusion (3 h) model was employed in 31 rabbits. Of these, 12 rabbits received the fusion protein (Fv-HSP72) intravenously. The remaining 19 control rabbits received a molar equivalent of 3E10Fv alone (n = 6), HSP72 alone (n = 6), or phosphate buffered saline (n = 7). Serial echocardiographic examinations were performed to assess left ventricular (LV) function before and after reperfusion. Micro-single photon emission computed tomography imaging of 99mTc-labeled annexin-V was performed with micro-computed tomography to characterize apoptotic damage in vivo, followed by gamma counting of the excised myocardial specimens to quantify cell death. Histopathological characterization of the myocardial tissue, and sequential cardiac troponin I measurements were also undertaken. RESULTS Myocardial annexin-V uptake was 43% lower in the area at risk (p = 0.0003) in Fv-HSP72-treated rabbits compared to controls receiving HSP72 or 3E10Fv alone. During reperfusion, troponin I release was 42% lower and the echocardiographic LV ejection fraction 27% higher in the Fv-HSP72-treated group compared to controls. Histopathological analyses confirmed penetration of 3E10Fv-containing molecules into cardiomyocytes in vivo, and treatment with Fv-HSP72 showed fewer apoptotic nuclei compared to control rabbits. CONCLUSIONS A single-dose administration of Fv-HSP72 fusion protein at the time of reperfusion reduced myocardial apoptosis almost by half, and improved LV functional recovery following myocardial ischemia-reperfusion injury in rabbits. It might have a potential to serve as an adjunct to early reperfusion in the management of myocardial infarction.

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Heat shock protein 70 protects against seizure-induced neuronal cell death in the hippocampus following experimental status epilepticus via inhibition of nuclear factor-κB activation-induced nitric oxide synthase II expression

Cited by 38 publications

References 38 publications

Pycnogenol Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells Through Regulating NF-κB-iNOS Signaling Pathway

Pycnogenol Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells Through Regulating NF-κB-iNOS Signaling Pathway

The detection and role of heat shock protein 70 in various nondisease conditions and disease conditions: a literature review

Cardioprotective Effects of HSP72 Administration on Ischemia-Reperfusion Injury

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