Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells

Jung, Tae Woo; Hwang, Hwan-Jin; Hong, Ho Cheol; Choi, Hee Youn; Yoo, Hye Jin; Baik, Sei Hyun; Choi, Kyung Mook

doi:10.1016/j.mce.2014.04.012

Cited by 62 publications

(48 citation statements)

References 48 publications

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“…Alternatively, recent evidence suggests that RvD1 has direct antiapoptotic effects. RvD1 inhibits apoptosis caused by antibiotic-induced ER stress in liver cells 53 and also attenuates cigarette smokeeinduced cell death in murine macrophages by upregulating the expression of the antiapoptotic proteins B-cell lymphoma-2 and B-cell lymphoma-extra large. 54 Taken together, we suspect that the net reductions in oxidative stress and cell death are likely due to a combination of direct effects of RvD1 on apoptosis signaling pathways as well as reductions in the numbers of inflammatory cells.…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Hsiao

Thatcher

Colas

et al. 2015

The American Journal of Pathology

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Chronic obstructive pulmonary disease is characterized, in part, by chronic inflammation that persists even after smoking cessation, suggesting that a failure to resolve inflammation plays an important role in the pathogenesis of the disease. It is widely recognized that the resolution of inflammation is an active process, governed by specialized proresolving lipid mediators, including lipoxins, resolvins, maresins, and protectins. Here, we report that proresolving signaling and metabolic pathways are disrupted in lung tissue from patients with chronic obstructive pulmonary disease, suggesting that supplementation with proresolving lipid mediators might reduce the development of emphysema by controlling chronic inflammation. Groups of mice were exposed long-term to cigarette smoke and treated with the proresolving mediator resolvin D1. Resolvin D1 was associated with a reduced development of cigarette smokeeinduced emphysema and airspace enlargement, with concurrent reductions in inflammation, oxidative stress, and cell death. Interestingly, resolvin D1 did not promote the differentiation of M2 macrophages and did not promote tissue fibrosis. Taken together, our results suggest that cigarette smoking disrupts endogenous proresolving pathways and that supplementation with specialized proresolving lipid mediators is an important therapeutic strategy in chronic lung disease, especially if endogenous specialized proresolving lipid mediator signaling is impaired. (Am J Pathol 2015, 185: 3189e3201; http:// dx.doi.org/10.1016/j.ajpath.2015 Chronic obstructive pulmonary disease (COPD) is a major global health problem and a leading cause of death and disability. Tobacco smoking remains the major causative factor in the development of COPD; however, new evidence suggests that household air pollution from fuel used for indoor cooking and heating is also a significant cause.

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Section: Discussionmentioning

confidence: 99%

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Hsiao

Thatcher

Colas

et al. 2015

The American Journal of Pathology

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“…Complying with our results, studies have revealed that AT-RvD1 treatment after injury results in decreased hyperoxia-associated apoptotic markers in lung tissue 34 and RvD1 attenuated ER stress-induced apoptosis and also decreased caspase-3 activity in human hepatoma cells. 35 These effects may suggest that cells such as AEC2 cells, a kind of resident cells in lung tissue, in fact, may not be of the same function as those inflammatory cells such as neutrophils during injury.…”

Section: Discussionmentioning

confidence: 99%

“…35 We had tested the receptors of RvD1, ALX/FPR2, and GPR32 in the process and the RNA and protein expressions show significant increase even in LPS group. Thus, we concluded that the antiapoptotic Figure 6 Inhibition of cytokine and chemokine production by resolvinD1 (RvD1) in lipopolysaccharide (LPS)-stimulated alveolar epithelial type 2 cells (AEC2 cells).…”

Section: Discussionmentioning

confidence: 99%

“…There could be several signaling pathway involved in the antiapoptotic mechanism. It was believed that RvD1 can reduce ER stress-induced apoptosis through JNK pathway in HepG2 cells 35 as well as rescue macrophages from oxidative stress-induced apoptosis through PKA-mediated repression of NOX activation and upregulation of antiapoptotic protein expression. 32 Some researchers even suspected that CCR5 involved in apoptosis and others indicated it was related with PMNs apoptotic effect.…”

Section: Discussionmentioning

confidence: 99%

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ResolvinD1 reduces apoptosis and inflammation in primary human alveolar epithelial type 2 cells

Xie

Wang

Liu

et al. 2016

Laboratory Investigation

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1Lung epithelial apoptosis and inflammatory responses are important pathological processes in many pulmonary disorders. ResolvinD1 (RvD1), generated in inflammatory resolution processes, reduces inflammatory responses in animal models of lung diseases. The aim of this study was to investigate whether RvD1 attenuates apoptosis and proinflammatory responses in primary human alveolar epithelial type 2 cells (AEC2 cells) that are exposed to lipopolysaccharide (LPS) in vitro. We examined the percentage of apoptotic AEC2 cells by flow cytometry. The expression levels of cytokines and chemokines were determined by ELISA and microarray. The expression levels of molecular signaling modulators were evaluated by western blot. LPS-stimulated AEC2 cells pretreated with RvD1 exhibited a statistically significant reduction in apoptosis. The pretreatment of LPS-stimulated cells with RvD1 stimulated the phosphorylation of AKT and prevented the cleavage of caspase-3, the upregulation of Bax, and the downregulation of Bcl-2. The antiapoptotic effects of RvD1 were abrogated upon pretreatment with a PI3K inhibitor. In addition, RvD1 reduced the release of cytokines and chemokines, and inhibited the degradation and phosphorylation of IκB-α in LPS-stimulated AEC2 cells. RvD1 reduces apoptosis of LPS-exposed AEC2 cells by inducing the phosphorylation of AKT and attenuates the inflammatory response by suppressing the degradation and phosphorylation of IκB-α.

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“…Adiponectin strongly upregulated CMKLR1 in primary human hepatocytes and in liver tissue while hepatic CMKLR1 was suppressed in the liver of adiponectin deficient mice (86). A recent study showed that pretreatment with resolvin D1 attenuated endoplasmic reticulum stress-induced apoptosis and decreased caspase 3 activity in HepG2 cells (87). These studies suggest that EPA and DHA derived pro-resolution mediators may have a role in reversing the metabolic and inflammatory disturbances seen in NAFLD and they support a role for cell and tissue enrichment in the precursor n-3 PUFAs.…”

Section: Omega-3 Fatty Acids and Resolution Of Inflammation In Nafld:mentioning

confidence: 99%

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

2016

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Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells

Cited by 62 publications

References 48 publications

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Resolvin D1 Reduces Emphysema and Chronic Inflammation

ResolvinD1 reduces apoptosis and inflammation in primary human alveolar epithelial type 2 cells

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

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