scholarly journals Skin Aging-Dependent Activation of the PI3K Signaling Pathway via Downregulation of PTEN Increases Intracellular ROS in Human Dermal Fibroblasts

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Eun-Mi Noh ◽  
Jinny Park ◽  
Hwa-Ryung Song ◽  
Jeong-Mi Kim ◽  
Minok Lee ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Ros Generation ◽  
Human Dermal Fibroblasts ◽  
Chronological Aging ◽  
Aged Skin ◽  
Pi3k Signaling Pathway ◽  
High Level

Reactive oxygen species (ROS) play a major role in both chronological aging and photoaging. ROS induce skin aging through their damaging effect on cellular constituents. However, the origins of ROS have not been fully elucidated. We investigated that ROS generation of replicative senescent fibroblasts is generated by the modulation of phosphatidylinositol 3,4,5-triphosphate (PIP3) metabolism. Reduction of the PTEN protein, which dephosphorylates PIP3, was responsible for maintaining a high level of PIP3 in replicative cells and consequently mediated the activation of the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway. Increased ROS production was blocked by inhibition of PI3K or protein kinase C (PKC) or by NADPH oxidase activating in replicative senescent cells. These data indicate that the signal pathway to ROS generation in replicative aged skin cells can be stimulated by reduced PTEN level. Our results provide new insights into skin aging-associated modification of the PI3K/NADPH oxidase signaling pathway and its relationship with a skin aging-dependent increase of ROS in human dermal fibroblasts.

scholarly journals (−)-Loliolide Isolated from Sargassum horneri Abate UVB-Induced Oxidative Damage in Human Dermal Fibroblasts and Subside ECM Degradation

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 435
Author(s):  
Ilekuttige Priyan Shanura Fernando ◽  
Soo-Jin Heo ◽  
Mawalle Kankanamge Hasitha Madhawa Dias ◽  
Dissanayaka Mudiyanselage Dinesh Madusanka ◽  
Eui-Jeong Han ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Sargassum Horneri ◽  
Mitogen Activated Protein Kinase ◽  
Ros Generation ◽  
Protective Effects ◽  
Human Dermal Fibroblasts ◽  
Mitogen Activated Protein ◽  
Uvb Exposure

Ultraviolet (UV) B exposure is a prominent cause of skin aging and a contemporary subject of interest. The effects are progressing through the generation of reactive oxygen species (ROS) that alter cell signaling pathways related to inflammatory responses. The present study evaluates the protective effects of (7aR)-6-hydroxy-4,4,7a-trimethyl-6,7-dihydro-5H-1-benzofuran-2-one (HTT) isolated from the edible brown algae Sargassum horneri against UVB protective effects in human dermal fibroblasts (HDFs). HTT treatment dose-dependently suppressed intracellular ROS generation in HDFs with an IC50 of 62.43 ± 3.22 µM. HTT abated UVB-induced mitochondrial hyperpolarization and apoptotic body formation. Furthermore, UVB-induced activation of key nuclear factor (NF)-κB and mitogen-activated protein kinase signaling proteins were suppressed in HTT treated cells while downregulating pro-inflammatory cytokines (interleukin-1β, 6, 8, 33 and tumor necrosis factor-α). Moreover, HTT treatment downregulated matrix metalloproteinase1, 2, 3, 8, 9 and 13 that was further confirmed by the inhibition of collagenase and elastase activity. The evidence implies that HTT delivers protective effects against premature skin aging caused by UVB exposure via suppressing inflammatory responses and degradation of extracellular matrix (ECM) components. Extensive research in this regard will raise perspectives for using HTT as an ingredient in UV protective ointments.

scholarly journals UVA Exposure Combined with Glycation of the Dermis Are Two Catalysts for Skin Aging and Promotes a Favorable Environment to the Appearance of Elastosis

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Hervé Pageon ◽  
Hélène Zucchi ◽  
Sylvie Ricois ◽  
Philippe Bastien ◽  
Daniel Asselineau
Keyword(s):  
Protein Expression ◽  
Biological Effect ◽  
Skin Aging ◽  
Chronological Aging ◽  
Advanced Glycosylation End Products ◽  
Uva Irradiation ◽  
Inflammatory State ◽  
Aged Skin

Skin aging is the result of superimposed intrinsic (individual) and extrinsic (e.g., UV exposure or nutrition) aging. Previous works have reported a relationship between UV irradiation and glycation in the aging process, leading, for example, to modified radical species production and the appearance of AGEs (advanced glycosylation end products) in increasing quantities, particularly glycoxidation products like pentosidine. In addition, the colocalization of AGEs and elastosis has also been observed. We first investigated the combination of the glycation reaction and UVA effects on a reconstructed skin model to explain their cumulative biological effect. We found that UVA exposure combined with glycation had the ability to intensify the response for specific markers: for example, MMP1 or MMP3 mRNA, proteases involved in extracellular matrix degradation, or proinflammatory cytokine, IL1α, protein expression. Moreover, the association of glycation and UVA irradiation is believed to promote an environment that favors the onset of an elastotic-like phenomenon: mRNA coding for elastin, elastase, and tropoelastin expression is increased. Secondly, because the damaging effects of UV radiation in vivo might be more detrimental in aged skin than in young skin due to increased accumulation of pentosidine and the exacerbation of alterations related to chronological aging, we studied the biological effect of soluble pentosidine in fibroblasts grown in monolayers. We found that pentosidine induced upregulation of CXCL2, IL8, and MMP12 mRNA expression (inflammatory and elastotic markers, respectively). Tropoelastin protein expression (elastin precursor) was also increased. In conclusion, fibroblasts in monolayers cultured with soluble pentosidine and tridimensional in vitro skin constructs exposed to the combination of AGEs and UVA promote an inflammatory state and an alteration of the dermal compartment in relation to an elastosis-like environment.

scholarly journals Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

2020 ◽  
Vol 21 (20) ◽  
pp. 7756
Author(s):  
Jung Hwan Oh ◽  
Fatih Karadeniz ◽  
Chang-Suk Kong ◽  
Youngwan Seo
Keyword(s):  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Nuclear Translocation ◽  
Quinic Acid ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Skin Damage ◽  
Chronological Aging

Cutaneous aging is divided into intrinsic and exogenous aging correspondingly contributing to the complex biological phenomenon in skin. Intrinsic aging is also termed chronological aging, which is the accumulation of inevitable changes over time and is largely genetically determined. Superimposed on this intrinsic process, exogenous aging is associated with environmental exposure, mainly to ultraviolet (UV) radiation and more commonly termed as photoaging. UV-induced skin aging induces increased expression of matrix metalloproteinases (MMPs) which in turn causes the collagen degradation. Therefore, MMP inhibitors of natural origin are regarded as a primary approach to prevent or treat photoaging. This study investigated the effects of 3,5-dicaffeoyl-epi-quinic acid (DEQA) on photoaging and elucidated its molecular mechanisms in UVA-irradiated human dermal fibroblasts (HDFs). The results show that treatment with DEQA decreases MMP-1 production and increases type I collagen production in UVA-damaged HDFs. In addition, treatment of UVA-irradiated HDFs with DEQA downregulates MMP-1, MMP-3 and MMP-9 expression via blocking MAPK-cascade-regulated AP-1 transcriptional activity in UVA-irradiated HDFs. Furthermore, DEQA relieves the UVA-mediated suppression of type I procollagen and collagen expression through stimulating TGF-β/Smad signaling, leading to activation of the Smad 2/3 and Smad 4 nuclear translocation. These results suggest that DEQA could be a potential cosmetic agent for prevention and treatment of skin photoaging.

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.

Protective effects of galangin against H 2 O 2 ‐induced aging via the IGF‐1 signaling pathway in human dermal fibroblasts

2019 ◽  
Vol 35 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Su‐Ying Wen ◽  
Jia‐Yi Chen ◽  
Chih‐Jung Chen ◽  
Chih‐Yang Huang ◽  
Wei‐Wen Kuo
Keyword(s):  
Signaling Pathway ◽  
Dermal Fibroblasts ◽  
Protective Effects ◽  
Human Dermal Fibroblasts

scholarly journals Photoprotective Effects of a Hyperoside-Enriched Fraction Prepared from Houttuynia cordata Thunb. on Ultraviolet B-Induced Skin Aging in Human Fibroblasts through the MAPK Signaling Pathway

Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2628
Author(s):  
Sariya Mapoung ◽  
Sonthaya Umsumarng ◽  
Warathit Semmarath ◽  
Punnida Arjsri ◽  
Kamonwan Srisawad ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Human Fibroblasts ◽  
Mapk Signaling ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Mapk Signaling Pathway ◽  
Ultraviolet B ◽  
Type I ◽  
Houttuynia Cordata ◽  
Houttuynia Cordata Thunb

Ultraviolet-B (UVB) irradiation causes skin damage via deleterious effects including oxidative stress, inflammation, and collagen degradation. The photoprotective effects of a hyperoside-enriched fraction obtained from Houttuynia cordata Thunb. (H. cordata) on the attenuation of UVB-induced skin aging in human fibroblasts were investigated. The solvent-partition technique was used to establish the hyperoside-enriched fraction of H. cordata (HcEA). The active compounds identified in the H. cordata extracts were hyperoside, quercitrin, chlorogenic acid, and rutin. With regard to the photoprotective effects of H. cordata on UVB-irradiated dermal fibroblasts, HcEA and hyperoside inhibited intracellular ROS production and inflammatory cytokine secretions (IL-6 and IL-8), while increasing collagen type I synthesis along with downregulating MMP-1 gene and protein expressions. Mechanistically, the hyperoside-enriched fraction obtained from H. cordata inhibited UVB-irradiated skin aging through regulation of the MAPK signaling pathway by attenuating the activation of JNK/ERK/c-Jun in human dermal fibroblasts. The hyperoside-enriched fraction of H. cordata exerted potent anti-skin aging properties against UVB exposure. The findings of this study can be applied in the cosmetics industry, as H. cordata extract can potentially be used in pharmaceutical or cosmetic formulations as a photoprotective or anti-skin aging agent.

scholarly journals NADPH oxidase is a novel target of delphinidin for the inhibition of UVB-induced MMP-1 expression in human dermal fibroblasts

2013 ◽  
Vol 22 (6) ◽  
pp. 428-430 ◽  
Author(s):  
Tae-Gyu Lim ◽  
Sung Keun Jung ◽  
Jong-eun Kim ◽  
Yoona Kim ◽  
Hyong Joo Lee ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Novel Target
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