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Zhou, Bingrong; Zhang, Mengli; Zhang, Qian; Permatasari, Felicia; Xu, Yang; Wu, Di; Yin, Zhiqiang; Luo, Dan

doi:10.1155/2013/530429

Cited by 80 publications

(60 citation statements)

References 41 publications

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“…Palmitic acid was recently reported to induce an upregulation of inflammatory factors such as interleukin-6 and tumor necrosis factor-α [30]. In our study, PC (16:0/16:0) was increased in the lymphoid stroma, especially the folliculus lymphaticus, in the War-T region.…”

Section: Discussionsupporting

confidence: 64%

Increased phosphatidylcholine (16:0/16:0) in the folliculus lymphaticus of Warthin tumor

Takizawa

Hayasaka

et al. 2014

Anal Bioanal Chem

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Warthin tumor (War-T), the second most common benign salivary gland tumor, consists mainly of neoplastic epithelium and lymphoid stroma. Some proteins and genes thought to be involved in War-T were evaluated by molecular biology and immunology. However, lipids as an important component of many tumor cells have not been well studied in War-T. To elucidate the molecular biology and pathogenesis of War-T, we investigated the visualized distribution of phosphatidylcholines (PCs) by imaging mass spectrometry (IMS). In our IMS analysis of a typical case, 10 signals were significantly different in intensity (p < 0.01) between the War-T and non-tumor (Non-T) regions. Five specific PCs were frequently found in the War-T regions of all of the samples: [PC (16:0/16:0) + K]+ (m/z 772.5), [PC (16:0/20:4) + K]+ (m/z 820.5), [PC (16:0/20:3) + K]+ (m/z 822.5), [PC (18:2/20:4) + K]+ (m/z 844.5), and [PC (18:0/20:5) + K]+ (m/z 846.5). PC (16:0/16:0) was increased specifically in the folliculus lymphaticus of War-T lymphoid stroma, suggesting a different metabolism. Localization of PC (16:0/16:0) might reflect inflammation activity participating in the pathogenesis of War-T. Thus, our IMS analysis revealed the profile of PCs specific to the War-T region. The molecules identified in our study provide important information for further studies of War-T pathogenesis.

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Section: Discussionsupporting

confidence: 64%

Increased phosphatidylcholine (16:0/16:0) in the folliculus lymphaticus of Warthin tumor

Takizawa

Hayasaka

et al. 2014

Anal Bioanal Chem

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“…Sebocyte lipids and lipid-derived products can undergo peroxidation reactions which generate cytotoxic mediators (Tochio et al, 2009; Zouboulis, 2004). These lipid peroxides can also stimulate keratinocytes to produce pro-inflammatory mediators including prostaglandins, IL-1α and IL-6, as well as antioxidants such as heme oxygenase-1, catalase and glutathione S-transferase (Ottaviani et al, 2006; Zhou et al, 2013; Zouboulis et al, 2014). PPARα ligands have been reported to inhibit sebaceous gland lipogenesis (Downie et al, 2004) and this may be important in regulating sebocyte function following injury.…”

Section: Discussionmentioning

confidence: 99%

Mustard vesicants alter expression of the endocannabinoid system in mouse skin

Wohlman

Composto

Heck

et al. 2016

Toxicology and Applied Pharmacology

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Vesicants including sulfur mustard (SM) and nitrogen mustard (NM) are bifunctional alkylating agents that cause skin inflammation, edema and blistering. This is associated with alterations in keratinocyte growth and differentiation. Endogenous cannabinoids, including N-arachidonoylethanolamine (anandamide, AEA) and 2-arachidonoyl glycerol (2-AG), are important in regulating inflammation, keratinocyte proliferation and wound healing. Their activity is mediated by binding to cannabinoid receptors 1 and 2 (CB1 and CB2), as well as peroxisome proliferator-activated receptor alpha (PPARα). Levels of endocannabinoids are regulated by fatty acid amide hydrolase (FAAH). We found that CB1, CB2, PPARα and FAAH were all constitutively expressed in mouse epidermis and dermal appendages. Topical administration of NM or SM, at concentrations that induce tissue injury, resulted in upregulation of FAAH, CB1, CB2 and PPARα, a response that persisted throughout the wound healing process. Inhibitors of FAAH including a novel class of vanillyl alcohol carbamates were found to be highly effective in suppressing vesicant-induced inflammation in mouse skin. Taken together, these data indicate that the endocannabinoid system is important in regulating skin homeostasis and that inhibitors of FAAH may be useful as medical countermeasures against vesicants.

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“…In addition, levels of IL-1β and IL-8 could be regulated by NF-κB pathway. Palmitic acid could induce human HaCaT keratinocytes to produce proinflammatory cytokines IL-6, IL-1β, and TNF-α in a dose-dependent manner via activation of NF-κB [15]. P. gingivalis induced IL-6, IL-8, and VCAM-1 expression in human gingival fibroblasts and human PDL cells through the NOD1/2-mediated NF-κB and ERK1/2 signaling pathways [16].…”

Section: Introductionmentioning

confidence: 99%

Nicotine Induces the Production of IL-1� and IL-8 via the a7 nAChR/NF-κB Pathway in Human Periodontal Ligament Cells: anin VitroStudy

Zhou

et al. 2014

Cell Physiol Biochem

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Background/Aims: Tobacco smoking is a major risk factor for the occurrence and progression of periodontitis. We previously demonstrated that nicotine could induce the expression of a7 nicotinic acetylcholine receptors (a7 nAChR) in human and rat periodontal tissues. To further examine the signal pathways mediated by a7 nAChR in periodontal ligament (PDL) cells, we investigated whether nicotine affects interleukin-1ß (IL-1ß) and interleukin-8 (IL-8) via the a7 nAChR/NF-κB pathway in human PDL cells. Methods: Human PDL cells were pre-incubated with alpha-bungarotoxin (a-BTX) or pyrrolidine dithiocarbamate (PDTC), then cultured with nicotine. Then, we used western blotting, a dual-luciferase reporter, real-time quantitative PCR and an enzyme-linked immunoassay to assess expression of the NF-κB p65 subunit, NF-κB activity and production of IL-1ß and IL-8 in human PDL cells. Results: Compared with the control group, nicotine could significantly induce production of IL-1ß and IL-8 in human PDL cells and cause the similar effects on the expression of the NF-κB p65 subunit and NF-κB activity. Conclusion: This study demonstrates that nicotine could induce production of IL-1ß and IL-8 via the a7 nAChR/NF-κB pathway in human PDL cells, providing data for a better understanding of the relationships among smoking, nicotine, and periodontitis.

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Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1β, and Tumor Necrosis Factor-αvia a NF-

Cited by 80 publications

References 41 publications

Increased phosphatidylcholine (16:0/16:0) in the folliculus lymphaticus of Warthin tumor

Increased phosphatidylcholine (16:0/16:0) in the folliculus lymphaticus of Warthin tumor

Mustard vesicants alter expression of the endocannabinoid system in mouse skin

Nicotine Induces the Production of IL-1� and IL-8 via the a7 nAChR/NF-κB Pathway in Human Periodontal Ligament Cells: anin VitroStudy

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