scholarly journals Decursin inhibits UVB-induced MMP expression in human dermal fibroblasts via regulation of nuclear factor-κB

2012 ◽  
Vol 31 (2) ◽  
pp. 477-483 ◽  
Author(s):  
BO-MI HWANG ◽  
EUN-MI NOH ◽  
JONG-SUK KIM ◽  
JEONG-MI KIM ◽  
JIN-KI HWANG ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Dermal Fibroblasts ◽  
Nuclear Factor ◽  
Human Dermal Fibroblasts

scholarly journals Epigallocatechin-3-gallate regulates cell growth, cell cycle and phosphorylated nuclear factor-κB in human dermal fibroblasts

2011 ◽  
Vol 32 (5) ◽  
pp. 637-646 ◽  
Author(s):  
Dong-Wook Han ◽  
Mi Hee Lee ◽  
Hak Hee Kim ◽  
Suong-Hyu Hyon ◽  
Jong-Chul Park
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Nuclear Factor Κb ◽  
Dermal Fibroblasts ◽  
Nuclear Factor ◽  
Human Dermal Fibroblasts

scholarly journals Acer tataricum subsp. ginnala Inhibits Skin Photoaging via Regulating MAPK/AP-1, NF-κB, and TGFβ/Smad Signaling in UVB-Irradiated Human Dermal Fibroblasts

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 662
Author(s):  
Yu-Jung Jin ◽  
Yura Ji ◽  
Young-Pyo Jang ◽  
Se-Young Choung
Keyword(s):  
Collagen Synthesis ◽  
Nuclear Factor Κb ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Nuclear Factor ◽  
Human Dermal Fibroblasts ◽  
Smad Pathway ◽  
Type I Procollagen ◽  
Skin Photoaging ◽  
Pro Inflammatory Cytokines

Skin, the organ protecting the human body from external factors, maintains structural and tensile strength by containing many collagen fibrils, particularly type I procollagen. However, oxidative stress by ultraviolet (UV) exposure causes skin photoaging by activating collagen degradation and inhibiting collagen synthesis. Acer tataricum subsp. ginnala extract (AGE) is a herbal medicine with anti-inflammatory and anti-oxidative effects, but there is no report on the protective effect against skin photoaging. Therefore, we conducted research concentrating on the anti-photoaging effect of Acer tataricum subsp. ginnala (AG) in UVB (20 mJ/cm2)-irradiated human dermal fibroblasts (HDF). Then, various concentrations (7.5, 15, 30 µg/mL) of AGE were treated in HDF for 24 h following UVB irradiation. After we performed AGE treatment, the matrix metalloproteinase1 (MMP1) expression was downregulated, and the type I procollagen level was recovered. Then, we investigated the mitogen-activated protein kinases/activator protein 1 (MAPK/AP-1) and nuclear factor-κB (NF-κB) pathway, which induce collagen breakdown by promoting the MMP1 level and pro-inflammatory cytokines. The results indicated that AGE downregulates the expression of the MAPK/AP-1 pathway, leading to MMP1 reduction. AGE inhibits nuclear translocation of NF-κB and inhibitor of nuclear factor-κB (IκB) degradation. Therefore, it downregulates the expression of MMP1 and pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 increased by UVB. Besides, the TGFβ/Smad pathway, which is mainly responsible for the collagen synthesis in the skin, was also analyzed. AGE decreases the expression of Smad7 and increases TGFβRII expression and Smad3 phosphorylation. This means that AGE stimulates the TGFβ/Smad pathway that plays a critical role in promoting collagen synthesis. Thus, this study suggests that AGE can be a functional material with anti-photoaging properties.

scholarly journals Growth factor regulation of hyaluronan synthesis and degradation in human dermal fibroblasts: importance of hyaluronan for the mitogenic response of PDGF-BB

2007 ◽  
Vol 404 (2) ◽  
pp. 327-336 ◽  
Author(s):  
Lingli Li ◽  
Trias Asteriou ◽  
Berit Bernert ◽  
Carl-Henrik Heldin ◽  
Paraskevi Heldin
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Dermal Fibroblasts ◽  
Mitogen Activated Protein Kinase ◽  
Signalling Pathways ◽  
Human Dermal Fibroblasts ◽  
High Level

The glycosaminoglycan hyaluronan is important in many tissuerepair processes. We have investigated the synthesis of hyaluronan in a panel of cell lines of fibroblastic and epithelial origin in response to PDGF (platelet-derived growth factor)-BB and other growth factors. Human dermal fibroblasts exhibited the highest hyaluronan-synthesizing activity in response to PDGF-BB. Analysis of HAS (hyaluronan synthase) and HYAL (hyaluronidase) mRNA expression showed that PDGF-BB treatment induced a 3-fold increase in the already high level of HAS2 mRNA, and increases in HAS1 and HYAL1 mRNA, whereas the levels of HAS3 and HYAL2 mRNA were not affected. Furthermore, PDGF-BB also increased the amount and activity of HAS2 protein, but not of HYAL1 and HYAL2 proteins. Using inhibitors for MEK1/2 [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase 1/2] (U0126) and for PI3K (phosphoinositide 3-kinase) (LY294002), as well as the SN50 inhibitor, which prevents translocation of the active NF-κB (nuclear factor κB) to the nucleus, we observed a complete inhibition of both HAS2 transcriptional activity and hyaluronan synthesis, whereas inhibitors of other signalling pathways were without any significant effect. TGF-β1 (transforming growth factor-β1) did not increase the activity of hyaluronan synthesis in dermal fibroblasts, but increased the activity of HYALs. Importantly, inhibition of hyaluronan binding to its receptor CD44 by the monoclonal antibody Hermes-1, inhibited PDGF-BB-stimulated [3H]thymidine incorporation of dermal fibroblasts. We conclude that the ERK MAPK and PI3K signalling pathways are necessary for the regulation of hyaluronan synthesis by PDGF-BB, and that prevention of its binding to CD44 inhibits PDGF-BB-induced cell growth.

scholarly journals Development of a Gene Delivery System of Oligonucleotides for Fibroses by Targeting Cell-Surface Vimentin-Expressing Cells with N-Acetylglucosamine-Bearing Polymer-Conjugated Polyethyleneimine

Polymers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1508
Author(s):  
Inu Song ◽  
Hirohiko Ise
Keyword(s):  
Cell Surface ◽  
Transforming Growth Factor ◽  
Stellate Cells ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Binding Activity ◽  
Dermal Fibroblasts ◽  
Cytoskeletal Proteins ◽  
Nuclear Factor ◽  
Factor Α

Targeting myofibroblasts and activated stellate cells in lesion sites of fibrotic tissues is an important approach to treat fibroses. Herein, we focused on targeting the cytoskeletal proteins vimentin, which are reportedly highly expressed on the surface of these cells and have N-acetylglucosamine (GlcNAc)-binding activity. A GlcNAc-bearing polymer synthesized via radical polymerization with a reversible addition-fragmentation chain transfer reagent has been previously found to interact with cell-surface vimentin-expressing cells. We designed a GlcNAc-bearing polymer-conjugated polyethyleneimine (PEI), as the gene carrier to target cell-surface vimentin-expressing cells and specifically deliver nuclear factor-κB decoy oligonucleotides (ODNs) and heat shock protein 47 (HSP47)-small interfering RNA (siRNA) to normal human dermal fibroblasts (NHDFs) that express cell-surface vimentin. The results showed that the expression of tumor necrosis factor-α in lipopolysaccharide-stimulated NHDFs and HSP47 in transforming growth factor-β1-stimulated NHDFs was suppressed by cellular uptake of the GlcNAc-bearing polymer-conjugated PEI/nuclear factor (NF)-κB decoy ODNs and HSP47-siRNA complexes through cell-surface vimentin, respectively. These findings suggest that the effective and specific delivery of ODNs and siRNA for cell-surface vimentin-expressing cells such as myofibroblasts and activated stellate cells can be achieved using GlcNAc-bearing polymer-conjugated PEI. This therapeutic approach could prove advantageous to prevent the promotion of various fibroses.

scholarly journals Serum amyloid A induces interleukin-6 in dermal fibroblasts via Toll-like receptor 2, interleukin-1 receptor-associated kinase 4 and nuclear factor-κB

Immunology ◽  
2014 ◽  
Vol 143 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Steven O'Reilly ◽  
Rachel Cant ◽  
Marzena Ciechomska ◽  
James Finnigan ◽  
Fiona Oakley ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Serum Amyloid A ◽  
Interleukin 1 ◽  
Nuclear Factor Κb ◽  
Dermal Fibroblasts ◽  
Serum Amyloid ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2

scholarly journals Anti-Inflammatory Effect of ETAS®50 by Inhibiting Nuclear Factor-κB p65 Nuclear Import in Ultraviolet-B-Irradiated Normal Human Dermal Fibroblasts

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ken Shirato ◽  
Tomoko Koda ◽  
Jun Takanari ◽  
Takuya Sakurai ◽  
Junetsu Ogasawara ◽  
...  
Keyword(s):  
Uv Irradiation ◽  
Nuclear Import ◽  
Dermal Fibroblasts ◽  
Nuclear Factor ◽  
Human Dermal Fibroblasts ◽  
Protein Levels ◽  
Proinflammatory Responses ◽  
Normal Human ◽  
Anti Inflammatory ◽  
Normal Human Dermal Fibroblasts

Ultraviolet (UV) irradiation induces proinflammatory responses in skin cells, including dermal fibroblasts, accelerating premature skin aging (photoaging). ETAS 50, a standardized extract from theAsparagus officinalisstem, is a novel and unique functional food that suppresses proinflammatory responses of hydrogen peroxide-stimulated skin fibroblasts and interleukin- (IL-) 1β-stimulated hepatocytes. To elucidate its antiphotoaging potencies, we examined whether ETAS 50 treatment after UV-B irradiation attenuates proinflammatory responses of normal human dermal fibroblasts (NHDFs). UV-B-irradiated NHDFs showed reduced levels of the cytosolic inhibitor of nuclear factor-κBα(IκBα) protein and increased levels of nuclear p65 protein. The nuclear factor-κB nuclear translocation inhibitor JSH-23 abolished UV-B irradiation-induced IL-1βmRNA expression, indicating that p65 regulates transcriptional induction. ETAS 50 also markedly suppressed UV-B irradiation-induced increases in IL-1βmRNA levels. Immunofluorescence analysis revealed that ETAS 50 retained p65 in the cytosol after UV-B irradiation. Western blotting also showed that ETAS 50 suppressed the UV-B irradiation-induced increases in nuclear p65 protein. Moreover, ETAS 50 clearly suppressed UV-B irradiation-induced distribution of importin-αprotein levels in the nucleus without recovering cytosolic IκBαprotein levels. These results suggest that ETAS 50 exerts anti-inflammatory effects on UV-B-irradiated NHDFs by suppressing the nuclear import machinery of p65. Therefore, ETAS 50 may prevent photoaging by suppressing UV irradiation-induced proinflammatory responses of dermal fibroblasts.

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