Ligation of CD40 receptor in human B lymphocytes triggers the 5-lipoxygenase pathway to produce reactive oxygen species and activate p38 MAPK

Ha, Yun Jung; Seul, Hee Jung; Lee, Jong Ran

doi:10.3858/emm.2011.43.2.012

Cited by 23 publications

(13 citation statements)

References 45 publications

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“…Numerous studies have stated that HSP70 mediated cell apoptosis through inhibition of JNK phosphorylation. When the redox balance is disturbed, HSP70 activates JNK phosphorylation, and the MAPK signaling pathway is activated, triggering a series of downstream signal responses (45). In the present study, phosphorylated JNK and p38 were increased in response to curcumin, whereas ERK was reduced in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 53%

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Yao

Lin

Wang

et al. 2015

International Journal of Molecular Medicine

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Abstract. Curcumin has been found to exhibit anticancer activity and certain studies have shown that curcumin triggers the apoptosis of human A549 lung adenocarcinoma cells. However, the mechanism underlying curcumin-mediated apoptosis is not completely understood. The present study was designed to investigate the effect of curcumin on the induction of apoptosis and apoptosis-related factors in human A549 lung adenocarcinoma cells. Treatment of A549 cells with curcumin caused a concentration-dependent inhibition of cell growth and an increase in apoptosis, as confirmed by THE MTT assay, flow cytometry and morphology analysis. Curcumin-treatment of A549 cells induced a loss of the mitochondrial membrane potential and increased cytosolic cytochrome c. Furthermore, curcumin-induced apoptosis was accompanied by changes in intracellular oxidative stress-related enzymes, including decreased intracellular reactive oxygen species levels, increased superoxide dismutase and decreased malondialdehyde and 4-hydroxynonenal. In addition, induction of apoptosis was also accompanied by phosphorylation and activation of mitogen-activated protein kinase signaling pathway factors c-Jun N-terminal kinase, p38 and extracellular signal-regulated kinase. IntroductionLung cancer is the main leading cause of cancer-related fatality worldwide, with a rapidly increasing rate in China and other Asian countries (1-4). Chemotherapy is currently the most frequently used treatment for lung cancer and other types of cancer. However, while this method of treatment kills cancer cells, it also destroys some normal cells. Thus, the identification of novel natural compounds with low toxicity and high selectivity for killing cancer cells is a significant area in cancer research (5), and several natural products have been used as alternative treatments for cancer (6,7).Curcumin, a natural and crystalline compound isolated from the plant Curcuma longa, has been widely studied for its anti-inflammatory, antiangiogenic, antioxidant and anticancer effects in Chinese systems of medicine (8,9). Additionally, previous studies have shown that curcumin exhibits antiproliferative and anticarcinogenic properties in a wide variety of cell lines and animals (10,11). Previous studies have demonstrated that curcumin inhibits the growth and apoptosis of human A549 lung adenocarcinoma cells (12)(13)(14). However, the mechanisms of curcumin-induced apoptosis via oxidative stress remain unclear.The physiological status of the reactive oxygen species (ROS) levels can regulate cell proliferation: When intracellular ROS levels are above a certain threshold, ROS inhibit the cell cycle, leading to increased cell apoptosis and necrosis. In the tumor cells it often maintains a higher state of oxidation, with higher levels of oxygen free radicals and lower levels of the antioxidant enzyme activity. This higher oxidation state can activate certain transcription factors and associated genes, such as NF-κB and API, thus, ensuring the survival, proliferation and migration of tumor ...

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Section: Discussionsupporting

confidence: 53%

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Yao

Lin

Wang

et al. 2015

International Journal of Molecular Medicine

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“…3A–3C ). These foci were also detected within 15 sec after irradiation, suggesting that they may arise due to rapid intracellular stress signals, possibly mediated by ROS [Bedard and Krause, 2007 ; Yalcin et al, 2010 ; Ha et al, 2011 ]. PARP-1 foci could be detected 3 min post-irradiation at low doses ( Fig.…”

Section: Resultsmentioning

confidence: 99%

XRCC1 coordinates disparate responses and multiprotein repair complexes depending on the nature and context of the DNA damage

Hanssen-Bauer

Solvang-Garten

Sundheim

et al. 2011

Environ. Mol. Mutagen.

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XRCC1 is a scaffold protein capable of interacting with several DNA repair proteins. Here we provide evidence for the presence of XRCC1 in different complexes of sizes from 200 to 1500 kDa, and we show that immunoprecipitates using XRCC1 as bait are capable of complete repair of AP sites via both short patch (SP) and long patch (LP) base excision repair (BER). We show that POLβ and PNK colocalize with XRCC1 in replication foci and that POLβ and PNK, but not PCNA, colocalize with constitutively present XRCC1-foci as well as damage-induced foci when low doses of a DNA-damaging agent are applied. We demonstrate that the laser dose used for introducing DNA damage determines the repertoire of DNA repair proteins recruited. Furthermore, we demonstrate that recruitment of POLβ and PNK to regions irradiated with low laser dose requires XRCC1 and that inhibition of PARylation by PARP-inhibitors only slightly reduces the recruitment of XRCC1, PNK, or POLβ to sites of DNA damage. Recruitment of PCNA and FEN-1 requires higher doses of irradiation and is enhanced by XRCC1, as well as by accumulation of PARP-1 at the site of DNA damage. These data improve our understanding of recruitment of BER proteins to sites of DNA damage and provide evidence for a role of XRCC1 in the organization of BER into multiprotein complexes of different sizes. Environ. Mol. Mutagen. 2011. © 2011 Wiley-Liss, Inc.

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“…Serum MPO levels were correlated with restenosis and atherosclerotic lesions [92]. Activation of the lipoxygenase and cyclooxygenase signaling pathways is also coupled with activation of NOX2 [31,32,108,109].…”

Section: Conclusion: Ros Atherosclerosis and Some Related Points Of mentioning

confidence: 99%

“…In phagosomes, superoxide interacts with chloride ions under catalytic control of myeloperoxidase, with production of hypochlorite [30]. Activation of the lipoxygenase signaling pathway is also coupled with activation of NOX2, when ligands CD154 or CD40L interact with CD40 of В lymphocytes [31,32].…”

Section: Nadph-oxidasesmentioning

confidence: 99%

Reactive Oxygen Species in Pathogenesis of Atherosclerosis

Гончаров¹,

Авдонин²,

Nadeev³

et al. 2015

CPD

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The volume of publications on the role of reactive oxygen species (ROS) in biological processes has been increasing exponentially over the last decades. ROS in large amounts clearly have detrimental effects on cell physiology, whereas low concentrations of ROS are permanently produced in cells and play a role as signaling molecules. An imbalance in ROS production and defense mechanisms can lead to pathological vascular remodeling, atherosclerosis being among them. The aim of this review is to examine different sources of ROS from the point of view of their participation in pathogenesis of atherosclerosis and related cardiovascular risk. Among the possible sources of ROS discussed here are mitochondria, NADPH-oxidases, xanthine oxidase, peroxidases, NO-synthases, cytochrome P450, cyclooxygenases, lipoxygenases, and hemoglobin of red blood cells. A great challenge for future research is to establish interrelations, feedback and feed-forward regulation mechanisms of various sources of ROS in development of atherosclerosis and other vascular pathologies.

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Ligation of CD40 receptor in human B lymphocytes triggers the 5-lipoxygenase pathway to produce reactive oxygen species and activate p38 MAPK

Cited by 23 publications

References 45 publications

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

XRCC1 coordinates disparate responses and multiprotein repair complexes depending on the nature and context of the DNA damage

Reactive Oxygen Species in Pathogenesis of Atherosclerosis

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