Genome-wide analysis of gene expression by crotonaldehyde in human umbilical vein endothelial cells

Jeong, Seong Il; Lee, Seung Eun; Yang, Hana; Park, Cheung Seog; Cho, Jeong Je; Park, Yong Seek

doi:10.1007/s13273-011-0017-x

Cited by 10 publications

(3 citation statements)

References 33 publications

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“…There is increasing evidence that α,β-unsaturated aldehydes in CS, including acrolein and crotonaldehyde play an important pathophysiological role in vascular diseases such as atherosclerosis and Alzheimer's disease. Exposure to α,β-unsaturated aldehydes is critical to the inflammatory response via activation of the proinflammatory signaling pathway and redox-sensitive transcription factors [27,28] . Furthermore, α,β-unsaturated aldehydes increase oxidative stress [29] , which plays a crucial role in the pathogenesis of vascular diseases via direct injury to the endothelium [30] .…”

Section: Discussionmentioning

confidence: 99%

Korean Red Ginseng water extract inhibits COX-2 expression by suppressing p38 in acrolein-treated human endothelial cells

Lee

Park

2014

Journal of Ginseng Research

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Cigarette smoke is considered a major risk factor for vascular diseases. There are many toxic compounds in cigarette smoke, including acrolein and other α,β-unsaturated aldehydes, which are regarded as mediators of inflammation and vascular dysfunction. Furthermore, recent studies have revealed that acrolein, an α,β-unsaturated aldehyde in cigarette smoke, induces inflammatory mediator expression, which is known to be related to vascular diseases. In this study, we investigated whether Korean Red Ginseng (KRG) water extract suppressed acrolein-induced cyclooxygenase (COX)-2 expression in human umbilical vein endothelial cells (HUVECs). Acrolein-induced COX-2 expression was accompanied by increased levels of phosphorylated p38 in HUVECs and KRG inhibited COX-2 expression in HUVECs. These results suggest that KRG suppresses acrolein-induced COX-2 expression via inhibition of the p38 mitogen-activated protein kinase signaling pathway. In addition, KRG exhibited an inhibitory effect on acrolein-induced apoptosis, as demonstrated by annexin V–propidium iodide staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay. Consistent with these results, KRG may exert a vasculoprotective effect through inhibition of COX-2 expression in acrolein-stimulated human endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Korean Red Ginseng water extract inhibits COX-2 expression by suppressing p38 in acrolein-treated human endothelial cells

Lee

Park

2014

Journal of Ginseng Research

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“…Total RNA was extracted from dorsal skin lesions using the TRIzol (ambion, 15596026) method [ 31 ]. RNA (1 µg) was used as a template to synthesize cDNA.…”

Section: Methodsmentioning

confidence: 99%

Calcium-Based Antimicrobial Peptide Compounds Attenuate DNFB-Induced Atopic Dermatitis-Like Skin Lesions via Th-Cells in BALB/c Mice

Wang

et al. 2022

IJMS

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Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease, characterized by severe itching and recurrent skin lesions. We hypothesized that a novel treatment involving calcium-based antimicrobial peptide compounds (CAPCS), a combination of natural calcium extracted from marine shellfish, and a variety of antimicrobial peptides, may be beneficial for AD. We established a dinitrofluorobenzene (DNFB)-induced AD model in BALB/c mice to test our hypothesis. We observed mouse behavior and conducted histopathological and immunohistochemical analyses on skin lesions before and after CAPCS treatment. We also characterized the changes in the levels of cytokines, inflammatory mediators, and Toll-like receptors (TLRs) in plasma and skin lesions. The results showed that (i) topical application of CAPCS ameliorated AD-like skin lesions and reduced scratching behavior in BALB/c mice; (ii) CAPCS suppressed infiltration of inflammatory cells and inhibited the expression of inflammatory cytokines in AD-like skin lesions; (iii) CAPCS reduced plasma levels of inflammatory cytokines; and (iv) CAPCS inhibited TLR2 and TLR4 protein expression in skin lesions. Topical application of CAPCS exhibits a therapeutic effect on AD by inhibiting inflammatory immune responses via recruiting helper T cells and engaging the TLR2 and TLR4 signaling pathways. Therefore, CAPCS may be useful for the treatment of AD.

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“…Several studies have revealed that crotonaldehyde reduces glutathione (GSH) levels and enhances the levels of intracellular reactive oxygen species (ROS), leading to a state of vulnerability in human airway cells [2] , [11] . Crotonaldehyde has been reported to modulate biological reactions by a variety of downstream signaling pathways [15] , [16] .…”

Section: Introductionmentioning

confidence: 99%

Induction of Heme Oxygenase-1 Inhibits Cell Death in Crotonaldehyde-Stimulated HepG2 Cells via the PKC-δ -p38 -Nrf2 Pathway

et al. 2012

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BackgroundCrotonaldehyde, an alpha, beta-unsaturated aldehyde present in cigarette smoke, is an environmental pollutant and a product of lipid peroxidation. It also produces adverse effects to humans and is considered as a risk factor for various diseases. Heme oxygenase-1 (HO-1) plays important roles in protecting cells against oxidative stress as a prime cellular defense mechanism. However, HO-1 may be associated with cell proliferation and resistance to apoptosis in cancer cells. The aim of this study was to examine the effects of HO-1 induction on cell survival in crotonaldehyde-stimulated human hepatocellular carcinoma (HepG2) cells.MethodsTo investigate the signaling pathway involved in crotonaldehyde-induced HO-1 expression, we compared levels of inhibition efficiency of specific inhibitors and specific small interfering RNAs (siRNAs) of several kinases. The cell-cycle and cell death was measured by FACS and terminal dUTP nick-end labeling (TUNEL) staining.ResultsTreatment with crotonaldehyde caused a significant increase in nuclear translocation of NF-E2 related factor (Nrf2). Treatment with inhibitors of the protein kinase C-δ (PKC-δ) and p38 pathways resulted in obvious blockage of crotonaldehyde-induced HO-1 expression. Furthermore, treatment with HO-1 siRNA and the specific HO-1 inhibitor zinc-protoporphyrin produced an increase in the G0/G1 phase of the cell cycle in crotonaldehyde-stimulated HepG2 cells.ConclusionsTaken together, the results support an anti-apoptotic role for HO-1 in crotonaldehyde-stimulated human hepatocellular carcinoma cells and provide a mechanism by which induction of HO-1 expression via PKC-δ–p38 MAPK–Nrf2 pathway may promote tumor resistance to oxidative stress.

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Genome-wide analysis of gene expression by crotonaldehyde in human umbilical vein endothelial cells

Cited by 10 publications

References 33 publications

Korean Red Ginseng water extract inhibits COX-2 expression by suppressing p38 in acrolein-treated human endothelial cells

Korean Red Ginseng water extract inhibits COX-2 expression by suppressing p38 in acrolein-treated human endothelial cells

Calcium-Based Antimicrobial Peptide Compounds Attenuate DNFB-Induced Atopic Dermatitis-Like Skin Lesions via Th-Cells in BALB/c Mice

Induction of Heme Oxygenase-1 Inhibits Cell Death in Crotonaldehyde-Stimulated HepG2 Cells via the PKC-δ -p38 -Nrf2 Pathway

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