Apamin inhibits TNF-α- and IFN-γ-induced inflammatory cytokines and chemokines via suppressions of NF-κB signaling pathway and STAT in human keratinocytes

Kim, Woon‐Hae; An, Hyun‐Jin; Kim, Jung-Yeon; Gwon, Mi‐Gyeong; Gu, Hyemin; Lee, Sunjae; Park, Ji Y.; Park, Joon Soo; Han, Sang‐Mi; Kim, Minkyung

doi:10.1016/j.pharep.2017.04.006

Cited by 39 publications

(53 citation statements)

References 41 publications

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“…Treatment with apamin in lipopolysaccharide (LPS)-treated THP-1-derived macrophages inhibited inflammatory responses due to a decrease in the NF-κB signal pathway. Similarly, some studies have demonstrated that apamin treatment effectively downregulates the NF-kB signaling pathway and signal transducers and activators of transcription (STAT) in vitro, thereby inhibiting pro-inflammatory cytokines and Th2 lymphocyte chemokines [13,15]. Kim et al [13] showed that intracellular lipid levels are inhibited by apamin in oxidized low-density lipoprotein (oxLDL)-treated macrophages.…”

Section: Atherosclerosismentioning

confidence: 99%

“…These channels play a pivotal role in various pathophysiological responses, such as atherosclerosis, Parkinson's disease, and hepatic fibrosis [11][12][13][14]. Kim et al [15] found that high concentrations (≥0.5 µg/mL) of apamin increase pro-inflammatory cytokines. A relatively low concentration of apamin has not been shown to affect cell death.…”

Section: Introductionmentioning

confidence: 99%

“…A relatively low concentration of apamin has not been shown to affect cell death. According to several studies, the proposed treatments use relatively low concentrations (1-10 µg/mL) of apamin injections [3,15]. Thus, it has been suggested that the therapeutic element does not have a toxicologic effect on target lesions.…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic Effects of Apamin as a Bee Venom Component for Non-Neoplastic Disease

Han

Park

2020

Toxins

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Bee venom is a natural toxin produced by honeybees and plays an important role in defending bee colonies. Bee venom has several kinds of peptides, including melittin, apamin, adolapamine, and mast cell degranulation peptides. Apamin accounts for about 2%-3% dry weight of bee venom and is a peptide neurotoxin that contains 18 amino acid residues that are tightly crosslinked by two disulfide bonds. It is well known for its pharmacological functions, which irreversibly block Ca2+-activated K+ (SK) channels. Apamin regulates gene expression in various signal transduction pathways involved in cell development. The aim of this study was to review the current understanding of apamin in the treatment of apoptosis, fibrosis, and central nervous system diseases, which are the pathological processes of various diseases. Apamin's potential therapeutic and pharmacological applications are also discussed.

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Section: Atherosclerosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Therapeutic Effects of Apamin as a Bee Venom Component for Non-Neoplastic Disease

Han

Park

2020

Toxins

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“…Keratinocytes contribute to the barrier functions of the epidermis through the formation of tight junctions and the stratum corneum and mediate inflammation through the secretion of cytokines, chemokines, and antibacterial peptides, and the expression of cellular adhesion molecules. 17,[36][37][38] Accordingly, we evaluated the inflammatory response of primary HEKs and human SCC cells to in vitro infection by C. t. bacteria. Cells treated with TNF, a typical inflammatory cytokine, served as a positive control for the induction of inflammatory genes.…”

Section: Upregulates the Mrna And Protein Levels Of Inflammatory Medimentioning

confidence: 99%

Corynebacterium tuberculostearicum, a human skin colonizer, induces the canonical nuclear factor‐κB inflammatory signaling pathway in human skin cells

Altonsy

Kurwa

Lauzon

et al. 2020

Immunity Inflam & Disease

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Introduction Corynebacterium tuberculostearicum (C. t.) is a ubiquitous bacterium that colonizes human skin. In contrast to other members of the genus Corynebacterium, such as toxigenic Corynebacterium diphtheriae or the opportunistic pathogen Corynebacterium jeikeium, several studies suggest that C. t. may play a role in skin health and disease. However, the mechanisms underlying these effects remain poorly understood. Methods To investigate whether C. t. induces inflammatory pathways in primary human epidermal keratinocytes (HEKs) and human cutaneous squamous carcinoma cells (SCCs), cell culture, reverse transcription‐polymerase chain reaction (PCR), enzyme‐linked immunosorbent assay, immunofluorescence microscopy, Western blot, chromatin immunoprecipitation‐PCR, small interfering RNA knockdown and luciferase reporter expression system were used. Results Herein, we demonstrate that C. t. upregulates the messenger RNA (mRNA) and protein levels of inflammatory mediators in two human skin cell lines, HEKs and SCCs. We further show activation of the canonical nuclear factor‐κB (NF‐κB) pathway in response to C. t. infection, including phosphorylation of the inhibitor of κB (IκB), the nuclear translocation of NF‐κB subunit (NF‐κB‐P65) and the recruitment of NF‐κB‐P65 and RNA polymerase to the NF‐κB response elements at the promoter region of the inflammatory genes. Lastly, the data confirm that C. t.‐induced tumor necrosis factor mRNA expression in HEKs is toll‐like receptor 2 (TLR2) dependent. Conclusion Our results offer a mechanistic model for C. t.‐induced inflammation in human keratinocytes via TLR2 and activation of IκB kinase and downstream signaling through the canonical NF‐κB pathway. Relevance to chronic inflammatory diseases of the skin and cutaneous oncology is discussed.

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“…To what extent this represents a paucity of keratinocytes in lesions, as opposed to specific down regulation of gene expression in keratinocytes within lesions, will require further investigation. Keratinocytes are known to play an important role in wound healing [45], are potent producers of IL10 and TGF [54], and have been shown to change to a sclerotic phenotype by gene silencing of Fli1 [55]. Although association of human CL and FLI1 [14,15] was not replicated here, Fli1 is a confirmed CL susceptibility gene in mice [56].…”

Section: Discussionmentioning

confidence: 74%

A genome-wide association study highlights a regulatory role forIFNG-AS1contributing to cutaneous leishmaniasis in Brazil

Almeida

Cherlin

et al. 2020

Preprint

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Background. Cutaneous leishmaniasis (CL) caused by Leishmania braziliensis remains animportant public health problem in Brazil. The goal of this study was to identify genetic risk factors for CL.Methods. Genome-wide analysis was undertaken using DNAs from 956 CL cases and 868 controls (phase 1) and 1110 CL cases and 1178 controls (phase 2) genotyped using Illumina HumanCoreExome BeadChips. Imputation against 1000G data provided 4,498,586 qualitycontrolled single nucleotide variants (SNVs) common across phase 1 and phase 2 samples.Linear mixed models in FastLMM were used to take account of genetic diversity/ethnicity/admixture. Cellular cytokines were measured using flow cytometry.

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Apamin inhibits TNF-α- and IFN-γ-induced inflammatory cytokines and chemokines via suppressions of NF-κB signaling pathway and STAT in human keratinocytes

Abstract: These results suggest that apamin has therapeutic effect on AD through improvement of inflammatory condition.

Cited by 39 publications

References 41 publications

Therapeutic Effects of Apamin as a Bee Venom Component for Non-Neoplastic Disease

Therapeutic Effects of Apamin as a Bee Venom Component for Non-Neoplastic Disease

Corynebacterium tuberculostearicum, a human skin colonizer, induces the canonical nuclear factor‐κB inflammatory signaling pathway in human skin cells

A genome-wide association study highlights a regulatory role forIFNG-AS1contributing to cutaneous leishmaniasis in Brazil

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