scholarly journals β-Ionone Attenuates Dexamethasone-Induced Suppression of Collagen and Hyaluronic Acid Synthesis in Human Dermal Fibroblasts

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 619
Author(s):  
Dabin Choi ◽  
Wesuk Kang ◽  
Soyoon Park ◽  
Bomin Son ◽  
Taesun Park
Keyword(s):  
Hyaluronic Acid ◽  
Mrna Expression ◽  
Glucocorticoid Receptors ◽  
Target Genes ◽  
Acid Synthesis ◽  
Collagen Type I ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts

Stress is a major contributing factor of skin aging, which is clinically characterized by wrinkles, loss of elasticity, and dryness. In particular, glucocorticoids are generally considered key hormones for promoting stress-induced skin aging through binding to glucocorticoid receptors (GRs). In this work, we aimed to investigate whether β-ionone (a compound occurring in various foods such as carrots and almonds) attenuates dexamethasone-induced suppression of collagen and hyaluronic acid synthesis in human dermal fibroblasts, and to explore the mechanisms involved. We found that β-ionone promoted collagen production dose-dependently and increased mRNA expression levels, including collagen type I α 1 chain (COL1A1) and COL1A2 in dexamethasone-treated human dermal fibroblasts. It also raised hyaluronic acid synthase mRNA expression and hyaluronic acid levels. Notably, β-ionone inhibited cortisol binding to GR, subsequent dexamethasone-induced GR signaling, and the expression of several GR target genes. Our results reveal the strong potential of β-ionone for preventing stress-induced skin aging and suggest that its effects are related to the inhibition of GR signaling in human dermal fibroblasts.

scholarly journals Air Pollution, Autophagy, and Skin Aging: Impact of Particulate Matter (PM10) on Human Dermal Fibroblasts

2018 ◽  
Vol 19 (9) ◽  
pp. 2727 ◽  
Author(s):  
Seo-Yeon Park ◽  
Eun Byun ◽  
Jeong Lee ◽  
Sungjoo Kim ◽  
Hei Kim
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Protein Expression ◽  
Mrna Expression ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Gene Analysis ◽  
World Health ◽  
Type I ◽  
Human Dermal Fibroblasts

A World Health Organization (WHO) report from 2016 states that over 3 million people die annually from air pollution, which places air pollution as the world’s largest single environmental health risk factor. Particulate matter (PM) is one of the main components of air pollution, and there is increasing evidence that PM exposure exerts negative effects on the human skin. To see the impact of air pollution on skin aging, we analyzed the effect of PM exposure on human dermal fibroblasts (HDFs) with Western blot, enzyme-linked immunosorbent assay (ELISA), and gene analysis. Cultured HDFs were exposed to PM10 at a concentration of 30 µg/cm2 for 24 h, and their gene/protein expression of inflammatory cytokines, fibroblast chemical mediators, and autophagy were assessed. A total of 1977 genes were found to be differentially expressed following PM exposure. We observed a significantly increased expression of pro-inflammatory genes interleukin (IL)-1β, IL-6, IL-8 and IL-33 in dermal fibroblasts exposed to PM10. Protein expression of IL-6 and IL-8 also significantly increased, which complemented our gene analysis results. In addition, there was a significant increase in cytochrome P450 (CYP1A1, CYP1B1), matrix metalloproteinase (MMP-1, MMP-3) mRNA expression, and significant decrease in transforming growth factor (TGF)-β, collagen type I alpha chain (COL1A1, COL1A2), and elastin (ELN) mRNA expression in PM-exposed dermal fibroblasts. Protein expression of MMP-1 was significantly increased and that of TGF-β and procollagen profoundly decreased, similar to the gene analysis results. Autophagy, an integrated cellular stress response, was also increased while transmission electron microscopy (TEM) analysis provided evidence of PM internalization in the autolysosomes. Taken together, our results demonstrate that PM10 contributes to skin inflammation and skin aging via impaired collagen synthesis. Increased autophagy in our study suggests a reparative role of autophagy in HDFs stressed with PM, but its biological significance requires further research.

scholarly journals Eisenia bicyclis Extract Repairs UVB-Induced Skin Photoaging In Vitro and In Vivo: Photoprotective Effects

Marine Drugs ◽  
2021 ◽  
Vol 19 (12) ◽  
pp. 693
Author(s):  
Se-In Choi ◽  
Hee-Soo Han ◽  
Jae-Min Kim ◽  
Geonha Park ◽  
Young-Pyo Jang ◽  
...  
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Epidermal Keratinocytes ◽  
Heme Oxygenase 1 ◽  
Type I ◽  
Skin Damage ◽  
Eisenia Bicyclis

Chronic exposure to ultraviolet B (UVB) is a major cause of skin aging. The aim of the present study was to determine the photoprotective effect of a 30% ethanol extract of Eisenia bicyclis (Kjellman) Setchell (EEB) against UVB-induced skin aging. By treating human dermal fibroblasts (Hs68) with EEB after UVB irradiation, we found that EEB had a cytoprotective effect. EEB treatment significantly decreased UVB-induced matrix metalloproteinase-1 (MMP-1) production by suppressing the activation of mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) signaling and enhancing the protein expression of tissue inhibitors of metalloproteinases (TIMPs). EEB was also found to recover the UVB-induced degradation of pro-collagen by upregulating Smad signaling. Moreover, EEB increased the mRNA expression of filaggrin, involucrin, and loricrin in UVB-irradiated human epidermal keratinocytes (HaCaT). EEB decreased UVB-induced reactive oxygen species (ROS) generation by upregulating glutathione peroxidase 1 (GPx1) and heme oxygenase-1 (HO-1) expression via nuclear factor erythroid-2-related factor 2 (Nrf2) activation in Hs68 cells. In a UVB-induced HR-1 hairless mouse model, the oral administration of EEB mitigated photoaging lesions including wrinkle formation, skin thickness, and skin dryness by downregulating MMP-1 production and upregulating the expression of pro-collagen type I alpha 1 chain (pro-COL1A1). Collectively, our findings revealed that EEB prevents UVB-induced skin damage by regulating MMP-1 and pro-collagen type I production through MAPK/AP-1 and Smad pathways.

scholarly journals Emodin induces collagen type I synthesis in Hs27 human dermal fibroblasts

2021 ◽  
Vol 21 (5) ◽  
Author(s):  
Parkyong Song ◽  
Han-Seul Jo ◽  
Wan-Seog Shim ◽  
Yang Kwon ◽  
Sungwon Bae ◽  
...  
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts

scholarly journals Anti-Aging Effects of Gyrophoric Acid on UVA-Irradiated Normal Human Dermal Fibroblasts

2020 ◽  
Vol 15 (4) ◽  
pp. 1934578X2091954
Author(s):  
Joong Hyun Shim
Keyword(s):  
Mrna Expression ◽  
Type I Collagen ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Aging Effects ◽  
Expression Levels ◽  
Normal Human ◽  
Normal Human Dermal Fibroblasts ◽  
Gyrophoric Acid

This research was conducted to identify the anti-aging effects of gyrophoric acid on the skin, using normal human dermal fibroblasts. The anti-aging effects of gyrophoric acid on dermal fibroblasts were demonstrated through cell viability, verification of collagen, type I, alpha 1 (COL1A1)/COL3A1/matrix metalloproteinases 1 (MMP1) messenger ribonucleic acid (mRNA) expression levels with quantitative real-time reverse-transcription polymerase chain reaction, and protein estimation using type I collagen/MMP1-enzyme-linked immunosorbent assay. Further, the effects of gyrophoric acid on superoxide dismutases (SODs)/catalase were investigated by assessing their mRNA expression. In ultraviolet A (UVA)-treated dermal fibroblasts, gyrophoric acid was observed to increase mRNA levels of COL1A1/COL3A1/SOD2 genes and type I collagen protein levels, consistent with its anti-aging role. Furthermore, gyrophoric acid treatment decreased both MMP1 mRNA and protein expression levels. Therefore, the results of this study demonstrate that gyrophoric acid can be considered as an important natural compound with potent anti-aging effects on the skin. Based on the findings of this study, further research about the mechanism of action of gyrophoric acid should be pursued so as to develop novel anti-aging strategies not only in the field of cosmetics but also for healthcare.

scholarly journals Prostaglandin E2 induces Skin Aging via E-prostanoid 1 in Normal Human Dermal Fibroblasts

2019 ◽  
Author(s):  
Joong Hyun Shim
Keyword(s):  
Prostaglandin E2 ◽  
Messenger Rna ◽  
Collagen Type ◽  
Collagen Type I ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Mrna Levels ◽  
Human Dermal Fibroblasts ◽  
Normal Human ◽  
Normal Human Dermal Fibroblasts

Collagen type I production decreases with aging, leading to wrinkles and impaired skin function. Prostaglandin E2 (PGE2), a lipid-derived signaling molecule produced from arachidonic acid by cyclo-oxygenase, inhibits collagen production and induces matrix metallopeptidase 1 (MMP1) expression by fibroblasts in vitro. PGE2-induced collagen expression inhibition and MMP1 promotion are aging mechanisms. This study investigated the role of E-prostanoid 1 (EP1) in PGE2 signaling in normal human dermal fibroblasts (NHDFs). When EP1 expression was inhibited by EP1 small interfering RNA (siRNA), there were no significant changes in messenger RNA (mRNA) levels of collagen, type I, alpha 1 (COL1A1)/MMP1 between siRNA-transfected NHDFs and siRNA-transfected NHDFs with PGE2. This result showed that EP1 is a PGE2 receptor. Extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation after PGE2 treatment significantly increased by ~2.5 times. In addition, PGE2 treatment increased the intracellular Ca2+ concentration in NHDFs. These results indicated that PGE2 is directly associated with EP1 pathway–regulated ERK1/2 and inositol trisphosphate (IP3) signaling in NHDFs.

scholarly journals AP Collagen Peptides Prevent Cortisol-Induced Decrease of Collagen Type I in Human Dermal Fibroblasts

2021 ◽  
Vol 22 (9) ◽  
pp. 4788
Author(s):  
Minjung Chae ◽  
Il-Hong Bae ◽  
Sung Hwan Lim ◽  
Kyoungmi Jung ◽  
Jonghwa Roh ◽  
...  
Keyword(s):  
Stress Responses ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Collagen Peptides ◽  
Wide Range ◽  
Dependent Inhibition

Cortisol is an endogenous glucocorticoid (GC) and primary stress hormone that regulates a wide range of stress responses in humans. The adverse effects of cortisol on the skin have been extensively documented but the underlying mechanism of cortisol-induced signaling is still unclear. In the present study, we investigate the effect of cortisol on collagen type I expression and the effect of AP collagen peptides, collagen tripeptide-rich hydrolysates containing 3% glycine-proline- hydroxyproline (Gly-Pro-Hyp, GPH) from the fish skin, on the cortisol-mediated inhibition of collagen type I and the cortisol-induced signaling that regulates collagen type I production in human dermal fibroblasts (HDFs). We determine that cortisol downregulates the expression of collagen type I. AP collagen peptides or GC receptor (GR) inhibitors recover the cortisol-mediated inhibition of collagen type I and GR activation. AP collagen peptides or GR inhibitors also prevent the cortisol-dependent inhibition of transforming growth factor (TGF)-β signaling. AP collagen peptides or GR inhibitors are effective in the prevention of collagen type I inhibition mediated by cortisol in senescent HDFs and reconstituted human skin models. Taken together, GR signaling might be responsible for the cortisol-mediated inhibition of TGF-β. AP collagen peptides act as GR-mediated signaling blockers, preventing the cortisol-dependent inhibition of collagen type I. Therefore, AP collagen peptides have the potential to improve skin health.

Involvement of phospholipase D1 in collagen type I production of human dermal fibroblasts

2006 ◽  
Vol 348 (4) ◽  
pp. 1398-1402 ◽  
Author(s):  
Kenji Ohguchi ◽  
Yoshiko Banno ◽  
Yukihiro Akao ◽  
Yoshinori Nozawa
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Phospholipase D1

scholarly journals Ulva intestinalis Protein Extracts Promote In Vitro Collagen and Hyaluronic Acid Production by Human Dermal Fibroblasts

Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2091 ◽  
Author(s):  
Justine Bodin ◽  
Amandine Adrien ◽  
Pierre-Edouard Bodet ◽  
Delphine Dufour ◽  
Stanislas Baudouin ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Acid Production ◽  
Biochemical Characterization ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Free Process ◽  
Ulva Intestinalis ◽  
Hyaluronic Acid Production

With the increase in life expectancy, reducing the visible signs of skin aging has become a major issue. A reduction in collagen and hyaluronic acid synthesis by fibroblasts is a feature of skin aging. The green seaweed, Ulva intestinalis, is an abundant and rich source of nutrients, especially proteins and peptides. The aim of this study was to assess the potential cosmetic properties of a protein fraction from Ulva intestinalis (PROT-1) containing 51% of proteins and 22% of polysaccharides, and its enzymatic peptide hydrolysates on human dermal fibroblasts. PROT-1 was extracted using a patented acid- and solvent-free process (FR2998894 (B1)). The biochemical characterization and chromatographic analysis showed a main set of proteins (25 kDa). To demonstrate the anti-aging potential of PROT-1, fibroblast proliferation and collagen and hyaluronic acid production were assessed on fibroblast cell lines from donors aged 20 years (CCD-1059Sk) and 46 years (CCD-1090Sk). PROT-1 induced a significant increase in collagen and hyaluronic acid production per cell, and a reduction in cell proliferation without increasing cell mortality. These effects were reversed after protein hydrolysis of PROT-1, showing the central role of proteins in this promising anti-aging property.

scholarly journals α-Ionone Protects Against UVB-Induced Photoaging in Human Dermal Fibroblasts

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1804 ◽  
Author(s):  
Tao Tong ◽  
Jinju Park ◽  
Youna Moon ◽  
Wesuk Kang ◽  
Taesun Park
Keyword(s):  
Hyaluronic Acid ◽  
Uv Light ◽  
Acid Synthesis ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Skin Damage ◽  
Smad Pathway ◽  
Naturally Occurring ◽  
Expression Of Genes ◽  
Tgf Β1

Ultraviolet (UV) light-induced wrinkle formation is a major dermatological problem and is associated with alteration in collagen. Here, we investigated the potential of α-ionone, a naturally occurring aromatic compound, in regulation of UVB-induced photoaging in human Hs68 dermal fibroblasts and identified the mechanisms involved. We found that in human dermal fibroblasts, α-ionone inhibited UVB-induced loss of collagen. α-Ionone upregulated the molecules participating in the TGF-β–SMAD pathway (TGF-β1, phospho-SMAD2/3, Col1A1, and Col1A2), but downregulated the molecules involved in the MAPK–AP-1 signaling pathway (phospho-p38, phospho-JNK, phospho-ERK, phospho-c-Fos, phospho-c-Jun, MMP1, MMP3, and MMP9), in human dermal fibroblasts. α-Ionone treatment also increased hyaluronic acid contents, and this effect was accompanied by an upregulation of mRNA expression of genes (HAS1 and HAS2) involved in hyaluronic acid synthesis. Thus, α-ionone is effective in the prevention of UVB-induced decrease of collagen and hyaluronic acid in human dermal fibroblasts. We propose that α-ionone may prove beneficial for the prevention of UV-induced wrinkle formation and skin damage.

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