Involvement of oxidative stress-mediated ERK1/2 and p38 activation regulated mitochondria-dependent apoptotic signals in methylmercury-induced neuronal cell injury

Lu, Tien Hui; Hsieh, Shan Yu; Yen, Cheng Chien; Wu, Hsi Chin; Chen, Kuo Liang; Hung, Dong-Zong; Chen, Chun Hung; Wu, Chin Ching; Su, Yi; Lin, Chen‐Yong; Liu, Shing‐Hwa; Huang, Chun Fa

doi:10.1016/j.toxlet.2011.04.013

Cited by 97 publications

(78 citation statements)

References 57 publications

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“…Although H 2 O 2 induced a decrease of E-cadherin protein expression in breast cancer cells [35] (Figure S2A in Additional file 4), these changes were only minimally affected by changes in PRDX1 expression. Also, H 2 O 2 induced only marginal or no changes in pThr202/pTyr204-MAPK (ERK1/2) and ERβ expression regardless of PRDX1 expression levels [36,37] (Figure 5). This is consistent with the selectivity of the association between PRDX1 and ER expression.…”

Section: Resultsmentioning

confidence: 99%

Peroxiredoxin-1 protects estrogen receptor α from oxidative stress-induced suppression and is a protein biomarker of favorable prognosis in breast cancer

et al. 2014

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IntroductionPeroxiredoxin-1 (PRDX1) is a multifunctional protein, acting as a hydrogen peroxide (H2O2) scavenger, molecular chaperone and immune modulator. Although differential PRDX1 expression has been described in many tumors, the potential role of PRDX1 in breast cancer remains highly ambiguous. Using a comprehensive antibody-based proteomics approach, we interrogated PRDX1 protein as a putative biomarker in estrogen receptor (ER)-positive breast cancer.MethodsAn anti-PRDX1 antibody was validated in breast cancer cell lines using immunoblotting, immunohistochemistry and reverse phase protein array (RPPA) technology. PRDX1 protein expression was evaluated in two independent breast cancer cohorts, represented on a screening RPPA (n = 712) and a validation tissue microarray (n = 498). In vitro assays were performed exploring the functional contribution of PRDX1, with oxidative stress conditions mimicked via treatment with H2O2, peroxynitrite, or adenanthin, a PRDX1/2 inhibitor.ResultsIn ER-positive cases, high PRDX1 protein expression is a biomarker of improved prognosis across both cohorts. In the validation cohort, high PRDX1 expression was an independent predictor of improved relapse-free survival (hazard ratio (HR) = 0.62, 95% confidence interval (CI) = 0.40 to 0.96, P = 0.032), breast cancer-specific survival (HR = 0.44, 95% CI = 0.24 to 0.79, P = 0.006) and overall survival (HR = 0.61, 95% CI = 0.44 to 0.85, P = 0.004). RPPA screening of cancer signaling proteins showed that ERα protein was upregulated in PRDX1 high tumors. Exogenous H2O2 treatment decreased ERα protein levels in ER-positive cells. PRDX1 knockdown further sensitized cells to H2O2- and peroxynitrite-mediated effects, whilst PRDX1 overexpression protected against this response. Inhibition of PRDX1/2 antioxidant activity with adenanthin dramatically reduced ERα levels in breast cancer cells.ConclusionsPRDX1 is shown to be an independent predictor of improved outcomes in ER-positive breast cancer. Through its antioxidant function, PRDX1 may prevent oxidative stress-mediated ERα loss, thereby potentially contributing to maintenance of an ER-positive phenotype in mammary tumors. These results for the first time imply a close connection between biological activity of PRDX1 and regulation of estrogen-mediated signaling in breast cancer.

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Section: Resultsmentioning

confidence: 99%

Peroxiredoxin-1 protects estrogen receptor α from oxidative stress-induced suppression and is a protein biomarker of favorable prognosis in breast cancer

et al. 2014

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“…Subsequently, the nuclear transcription factor NF-κB is phosphorylated and regulates the expressions of inflammation-related genes [23]. Furthermore, JNK might also promote apoptosis through the TNF-α-dependant pathway [34], which needs further research in the future. Western blot analysis for stomach tissues and cells demonstrated that all of the three signaling of MAPK are up-regulated in the mice model.…”

Section: Discussionmentioning

confidence: 99%

Protective activity of salidroside against ethanol-induced gastric ulcer via the MAPK/NF-κB pathway in vivo and in vitro

Chang

Luo

Jiang

et al. 2015

International Immunopharmacology

129

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“…331 This shift in HIF expression likely underlies the observation that under conditions of prolonged hypoxia the initial protective mechanisms of the kidney either fail to be engaged or are down-regulated. 292,334,335 Thus, the expression of proangiogenic factors such as VEGF-A isoform 164 is repressed, and the expression of dys-angiogenic factors such as VEGF-A isoforms 120 and 188 is increased, causing capillary rarefaction. 221,223,251,252 Fibrosis is driven by decreased expression of metalloproteinases and increased expression of their inhibitors and extracellular matrix proteins.…”

Section: The Hypoxia Death Cyclementioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

128

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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Involvement of oxidative stress-mediated ERK1/2 and p38 activation regulated mitochondria-dependent apoptotic signals in methylmercury-induced neuronal cell injury

Cited by 97 publications

References 57 publications

Peroxiredoxin-1 protects estrogen receptor α from oxidative stress-induced suppression and is a protein biomarker of favorable prognosis in breast cancer

Peroxiredoxin-1 protects estrogen receptor α from oxidative stress-induced suppression and is a protein biomarker of favorable prognosis in breast cancer

Protective activity of salidroside against ethanol-induced gastric ulcer via the MAPK/NF-κB pathway in vivo and in vitro

Hypoxia: The Force that Drives Chronic Kidney Disease

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