scholarly journals Anti‑apoptotic effects of glycosaminoglycans via inhibition of ERK/AP‑1 signaling in TNF‑α‑stimulated human dermal fibroblasts

2018 ◽  
Author(s):  
Jungtae Na ◽  
Dong‑Ho Bak ◽  
Song I Im ◽  
Hyangtae Choi ◽  
Jung Hyun Hwang ◽  
...  
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tnf Α ◽  
Apoptotic Effects

scholarly journals Efficacy of Alpinumisoflavone Isolated from Maclura tricuspidata Fruit in Tumor Necrosis Factor-α-Induced Damage of Human Dermal Fibroblasts

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 514
Author(s):  
Sullim Lee ◽  
Giang Do Hoang ◽  
Daeyoung Kim ◽  
Ho Sueb Song ◽  
Sungyoul Choi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Dermal Fibroblasts ◽  
The Body ◽  
Hazardous Substances ◽  
Human Dermal Fibroblasts ◽  
Cutaneous Lesions ◽  
Matrix Metalloproteinase 1 ◽  
Tnf Α ◽  
Necrosis Factor

The skin is an important organ in the human body that protects the body from environmentally hazardous substances. Reactive oxygen species (ROS) cause inflammatory reactions and degradation of the extracellular matrix leading to skin aging and various cutaneous lesions. This study evaluated the potential of isoflavones isolated from Maclura tricuspidata fruit to prevent TNF-α-induced skin inflammation in normal human dermal fibroblasts (HDFs). It focused on alpinumisoflavone (AIF) that suppressed the accumulation of ROS and nitric oxide (NO) in tumor necrosis factor-alpha (TNF-α)-treated HDFs. AIF inhibited the TNF-α-induced increase in matrix metalloproteinase-1, decreased procollagen I α1, and suppressed pro-inflammatory mediators and pro-inflammatory cytokines, including NO synthase, cyclooxygenase-2, interleukin (IL)-1β, IL-6, and IL-8 that trigger inflammatory responses. AIF inhibited nuclear factor-κB and activating protein 1 mitogen-activated protein kinases that were increased by TNF-α stimulation. These results suggest that AIF may protect skin from aging and various cutaneous lesions.

Isomenthone protects human dermal fibroblasts from TNF-α-induced death possibly by preventing activation of JNK and p38 MAPK

2012 ◽  
Vol 50 (10) ◽  
pp. 3514-3520 ◽  
Author(s):  
Eunsun Jung ◽  
Sangyo Byun ◽  
Seungbeom Kim ◽  
Moohan Kim ◽  
Deokhoon Park ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tnf Α

Up-regulation of ICAM-1 expression on human dermal fibroblasts by IFN β in the presence of TNF-α

FEBS Letters ◽  
1995 ◽  
Vol 363 (1-2) ◽  
pp. 141-144 ◽  
Author(s):  
Takashi Horikoshi ◽  
Kyori Ezoe ◽  
Hidemi Nakagawa ◽  
Hiroaki Eguchi ◽  
Niro Hanada ◽  
...  
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tnf Α

scholarly journals Primary Ciliogenesis by 2-Isopropylmalic Acid Prevents PM2.5-Induced Inflammatory Response and MMP-1 Activation in Human Dermal Fibroblasts and a 3-D-Skin Model

2021 ◽  
Vol 22 (20) ◽  
pp. 10941
Author(s):  
Ji-Eun Bae ◽  
Daejin Min ◽  
Ji Yeon Choi ◽  
Hyunjung Choi ◽  
Joon Bum Kim ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Primary Cilia ◽  
Dermal Fibroblasts ◽  
Oxygen Species ◽  
Human Dermal Fibroblasts ◽  
Skin Model ◽  
Skin Cells ◽  
Tnf Α ◽  
Stress Kinase ◽  
Pro Inflammatory Cytokines

Particulate matters (PMs) increase oxidative stress and inflammatory response in different tissues. PMs disrupt the formation of primary cilia in various skin cells, including keratinocytes and melanocytes. In this study, we found that 2-isopropylmalic acid (2-IPMA) promoted primary ciliogenesis and restored the PM2.5-induced dysgenesis of primary cilia in dermal fibroblasts. Moreover, 2-IPMA inhibited the generation of excessive reactive oxygen species and the activation of stress kinase in PM2.5-treated dermal fibroblasts. Further, 2-IPMA inhibited the production of pro-inflammatory cytokines, including IL-6 and TNF-α, which were upregulated by PM2.5. However, the inhibition of primary ciliogenesis by IFT88 depletion reversed the downregulated cytokines by 2-IPMA. Moreover, we found that PM2.5 treatment increased the MMP-1 expression in dermal fibroblasts and a human 3-D-skin model. The reduced MMP-1 expression by 2-IPMA was further reversed by IFT88 depletion in PM2.5-treated dermal fibroblasts. These findings suggest that 2-IPMA ameliorates PM2.5-induced inflammation by promoting primary ciliogenesis in dermal fibroblasts.

scholarly journals Alnus Sibirica Extracts Suppress the Expression of Inflammatory Cytokines Induced by Lipopolysaccharides, Tumor Necrosis Factor-α, and Interferon-γ in Human Dermal Fibroblasts

Molecules ◽  
2019 ◽  
Vol 24 (16) ◽  
pp. 2883 ◽  
Author(s):  
Jeongyoon Choi ◽  
Sunghee Moon ◽  
Hyemi Bae ◽  
Young-Won Kim ◽  
Donghee Lee ◽  
...  
Keyword(s):  
Immune Responses ◽  
Interferon Γ ◽  
Dermal Fibroblasts ◽  
Raw264.7 Cells ◽  
Human Dermal Fibroblasts ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Inflammatory Processes ◽  
Factor Α ◽  
Oxidative Effects

The effects of Alnus sibirica (AS) extracts on cytokine expression induced by inflammatory stimulants were examined in human dermal fibroblasts (HDFs) and RAW264.7 cells. The anti-oxidative effect and effect on cell viability of AS extracts were evaluated, and four extracts with the highest anti-oxidative effects were selected. HDFs and RAW264.7 cells were treated with inflammatory stimulants, and the expression of cytokines involved in acute (IL-6 and IL-10) and chronic (IL-18) inflammation, the initiation of the immune response (IL-33), and non-specific immune responses (IL-1β, IL-8, and TNF-α) were determined using a reverse-transcription polymerase chain reaction. LPS increased the expression of all the cytokines, except for IL-18; however, AS extracts, particularly AS2 and AS4, reduced this increase, and TNF-α treatment markedly increased the expression of cytokines related to non-specific immune responses. IFN-γ treatment induced no significant changes, except for increased IL-33 expression in HDFs. AS extracts inhibited the increase in the expression of IL-33 and other cytokines in HDFs. Thus, the exposure of HDFs and RAW264.7 cells to inflammatory stimulants increased the expression of cytokines related to all the inflammatory processes. HDFs are involved not only in simple tissue regeneration but also in inflammatory reactions in the skin. AS2 and AS4 may offer effective therapy for related conditions.

scholarly journals The transcription of human α1(I) procollagen gene (COL1A1) is suppressed by tumour necrosis factor-α through proximal short promoter elements: evidence for suppression mechanisms mediated by two nuclear-factorbinding sites

1996 ◽  
Vol 319 (3) ◽  
pp. 811-816 ◽  
Author(s):  
Kenichi MORI ◽  
Atsushi HATAMOCHI ◽  
Hiroaki UEKI ◽  
Anne OLSEN ◽  
Sergio A. JIMENEZ
Keyword(s):  
Promoter Activity ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Flanking Sequences ◽  
Substitution Mutations ◽  
Factor Α ◽  
Cat Gene ◽  
Necrosis Factor

Recent studies have demonstrated that tumour necrosis factor-α (TNF-α) decreases α1(I) procollagen gene (COL1A1) expression in cultured human dermal fibroblasts. The purpose of this study was to analyse the transcriptional control of COL1A1 by TNF-α. Cultured human dermal fibroblasts were transiently transfected with plasmids containing 5´ flanking sequences of COL1A1 fused to the chloramphenicol acetyltransferase (CAT) gene, and were incubated for 48 h in medium with or without TNF-α. TNF-α inhibited the CAT activity of fibroblasts transfected with plasmids containing 2.3 kb of 5´ flanking sequences of COL1A1, whereas the activity of control plasmids containing the herpes simplex thymidine kinase promoter gene (pBLCAT) was unaltered. A series of deletion constructs or various small substitution mutations of the COL1A1 5´ flanking region fused to the CAT gene were also transfected, and CAT activity was measured after incubation with TNF-α. TNF-α suppressed COL1A1 promoter activity through proximal short promoter elements containing only 107 bp. Short substitution mutations between -101 and -97 bp or between -46 and -38 bp abolished TNF-α suppression of COL1A1 promoter activity. DNA–protein complex formation was observed involving both sites in gel retardation assays. These results suggest that TNF-α suppressed COL1A1 promoter activity through elements located between -101 and -97 bp and between -46 and -38 bp of the COL1A1 promoter, and that the suppression involved DNA-protein interactions.

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