scholarly journals Hyaluronan – a key player or just a bystander in skin photoaging?

2021 ◽  
Author(s):  
Romana Šínová ◽  
Vojtěch Pavlík ◽  
Martin Ondrej ◽  
Vladimír Velebný ◽  
Kristina Nešporová
Keyword(s):  
Skin Photoaging

scholarly journals 4-Hydroxynonenal Contributes to Fibroblast Senescence in Skin Photoaging Evoked by UV-A Radiation

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 365 ◽  
Author(s):  
Audrey Swiader ◽  
Caroline Camaré ◽  
Paul Guerby ◽  
Robert Salvayre ◽  
Anne Negre-Salvayre
Keyword(s):  
Lipid Peroxidation ◽  
Dermal Fibroblasts ◽  
Connective Tissues ◽  
Hairless Mice ◽  
Cultured Fibroblasts ◽  
Γh2ax Foci ◽  
Skin Photoaging ◽  
Actinic Elastosis

Solar ultraviolet A (UV-A) radiation promotes a huge variety of damages on connective tissues and dermal fibroblasts, including cellular senescence, a major contributor of skin photoaging. The mechanisms of skin photoaging evoked by UV-A partly involve the generation of reactive oxygen species and lipid peroxidation. We previously reported that 4-hydroxynonenal (HNE), a lipid peroxidation-derived aldehyde, forms adducts on elastin in the skins of UV-A irradiated hairless mice, possibly contributing to actinic elastosis. In the present study, we investigated whether and how HNE promotes fibroblast senescence in skin photoaging. Dermal fibroblasts of skins from UV-A-exposed hairless mice exhibited an increased number of γH2AX foci characteristic of cell senescence, together with an accumulation of HNE adducts partly colocalizing with the cytoskeletal protein vimentin. Murine fibroblasts exposed to UV-A radiation (two cycles of 15 J/cm2), or HNE (30 µM, 4 h), exhibited senescence patterns characterized by an increased γH2AX foci expression, an accumulation of acetylated proteins, and a decreased expression of the sirtuin SIRT1. HNE adducts were detected on vimentin in cultured fibroblasts irradiated by UV-A or incubated with HNE. The HNE scavenger carnosine prevented both vimentin modification and fibroblast senescence evoked by HNE in vitro and in the skins of UV-A-exposed mice. Altogether, these data emphasize the role of HNE and lipid peroxidation-derived aldehydes in fibroblast senescence, and confirm the protective effect of carnosine in skin photoaging.

Lysophosphatidylcholine exerts an anti‐skin photoaging effect via heat shock protein 70 induction

2021 ◽  
Author(s):  
Hyunmin Hwang ◽  
Hyeyeon Chun ◽  
Daehyun Kim ◽  
Munju Shin ◽  
Yun‐Sun Kim ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Skin Photoaging

Druggable Targets for Skin Photoaging: Potential Application of Nanocosmetics and Nanomedicine

2011 ◽  
pp. 197-227
Author(s):  
Giselle Z. Justo ◽  
Sílvia M. Shishido ◽  
Daisy Machado ◽  
Rodrigo A. da Silva ◽  
Carmen V. Ferreira
Keyword(s):  
Potential Application ◽  
Skin Photoaging ◽  
Druggable Targets

scholarly journals UVA Photoprotective Activity of Brown Macroalgae Sargassum cristafolium

Biomedicines ◽  
2019 ◽  
Vol 7 (4) ◽  
pp. 77 ◽  
Author(s):  
Prasedya ◽  
Syafitri ◽  
Geraldine ◽  
Hamdin ◽  
Frediansyah ◽  
...  
Keyword(s):  
Uv Radiation ◽  
Cell Model ◽  
Positive Control ◽  
Uv Spectra ◽  
Protective Effects ◽  
Negative Effects ◽  
Brown Macroalgae ◽  
Uva Irradiation ◽  
Skin Photoaging

Sunscreens today contain several synthetic UV (Ultraviolet) filter molecules to protect the skin epidermis from UV radiation damage. However, these molecules may create several negative effects on human skin. Due to this condition, there is an increase in the development of natural products to replace uses of these synthetic chemicals. Brown macroalgae Sargassum has been recently studied for its photoprotective activities. The purpose of this study is to investigate photoprotective activity of one of most abundant Sargassum species in Lombok coast; Sargassum cristaefolium. Spectrophotometry analysis with UV-VIS revealed the UV spectra absorbing capability of Sargassum cristaefolium (SC) in the UVA spectrum range (314–400 nm). Furthermore, spectrometry analyses with LC-MS revealed the existence of UV absorbing compound MAA-palythene. In correlation, SC ethanol extracts also demonstrate that it could protect DNA from UVA irradiation as analyzed in vitro in HeLa cell model. The effects of SC on UVA exposed-dorsal mice skin have also shown interesting results, as mice pretreated with SC before UVA exposure showed protective activity on the epidermal integrity similar as positive control. Whereas, UV exposed mice without SC or commercial products resulted in increased epidermal thickness, which is the common parameter of skin photoaging. In addition, pretreated mice with SC also show protective effects in the formation of collagen connective tissues. Overall, current results show promising photoprotective activity of SC against UV radiation. More advanced investigations of SC as a potential photoprotective agent would be reasonable for development of macroalgae-based natural skin protection products.

scholarly journals Role of HYBID (Hyaluronan Binding Protein Involved in Hyaluronan Depolymerization), Alias KIAA1199/CEMIP, in Hyaluronan Degradation in Normal and Photoaged Skin

2019 ◽  
Vol 20 (22) ◽  
pp. 5804 ◽  
Author(s):  
Hiroyuki Yoshida ◽  
Yasunori Okada
Keyword(s):  
Binding Protein ◽  
Normal Skin ◽  
Collagen Fibers ◽  
Skin Fibroblasts ◽  
Photoaged Skin ◽  
Skin Photoaging ◽  
Skin Wrinkling ◽  
Initial Process ◽  
Hyaluronan Binding

Photoaged skin is characterized clinically by apparent manifestations such as wrinkles and sagging, and histologically by an accumulation of abnormal elastin and a severe loss of collagen fibers in the dermis. Quantitative and qualitative alterations in elastin and collagens are considered to be responsible for the formation of wrinkles and sagging. However, since the integrity of elastin and collagen fibers in the dermis is maintained by their interactions with hyaluronan (HA) and a proteoglycan network structure, HA degradation may be the initial process, prior to the breakdown of the fibrillary components, leading to wrinkles and sagging in photoaged skin. We have recently discovered a new HA-degrading mechanism mediated by HYBID (hyaluronan binding protein involved in hyaluronan depolymerization), alias KIAA1199/CEMIP, in human skin fibroblasts, and examined the implication of HYBID for skin photoaging. In this review, we give an overview of the characteristics of HYBID and its prospective roles in HA turnover in normal skin and excessive HA degradation in photoaged skin. In addition, we describe our data on the inhibition of HYBID activity and expression by plant extracts in skin fibroblasts; and propose novel strategies to prevent or improve photoaging symptoms, such as skin wrinkling, by inhibition of HYBID-mediated HA degradation.

scholarly journals Caffeic Acid Phenethyl Ester Inhibits UV-Induced MMP-1 Expression by Targeting Histone Acetyltransferases in Human Skin

2019 ◽  
Vol 20 (12) ◽  
pp. 3055 ◽  
Author(s):  
Eun Ju Shin ◽  
Seongin Jo ◽  
Hyo-kyoung Choi ◽  
Sungbin Choi ◽  
Sanguine Byun ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Human Skin ◽  
Ex Vivo ◽  
Bioactive Compound ◽  
Caffeic Acid Phenethyl Ester ◽  
Inhibitory Effect ◽  
Dermal Fibroblasts ◽  
Regulatory Pathways ◽  
Skin Photoaging ◽  
Hdf Cells

Caffeic acid phenethyl ester (CAPE), a naturally occurring bioactive compound, displays anti-inflammatory, anti-carcinogenic, and anti-microbial effects. However, the effect of CAPE on skin photoaging is unknown. Herein, we investigated the inhibitory effect of CAPE against ultraviolet (UV) irradiation-mediated matrix metalloproteinase (MMP)-1 expression and its underlying molecular mechanism. CAPE treatment suppressed UV-induced MMP-1 levels in both human dermal fibroblasts (HDF) and human skin tissues. While CAPE did not display any significant effects against the upstream regulatory pathways of MMP-1, CAPE was capable of reversing UV-mediated epigenetic modifications. CAPE suppressed UV-induced acetyl-histone H3 (Lys9) as well as total lysine acetylation in HDF cells. Similarly, CAPE also attenuated UV-induced lysine acetylations in human skin tissues, suggesting that the CAPE-mediated epigenetic alterations can be recapitulated in ex vivo conditions. CAPE was found to attenuate UV-induced histone acetyltransferase (HAT) activity in HDF. Notably, CAPE was able to directly inhibit the activity of several HATs including p300, CREP-binding protein (CBP), and p300/CBP-associated factor (PCAF), further confirming that CAPE can function as an epigenetic modulator. Thus, our study suggests that CAPE maybe a promising agent for the prevention of skin photoaging via targeting HATs.

scholarly journals Opuntiol Prevents Photoaging of Mouse Skin via Blocking Inflammatory Responses and Collagen Degradation

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
P. Veeramani kandan ◽  
Agilan Balupillai ◽  
G. Kanimozhi ◽  
Haseeb A. Khan ◽  
Abdullah S. Alhomida ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Mouse Skin ◽  
Skin Lesions ◽  
Tnf Α ◽  
Skin Photoaging ◽  
Dermal Collagen ◽  
Collagen Molecules ◽  
Experimental Mouse ◽  
Inflammatory Proteins ◽  
Uva Radiation

In the present study, we investigated the potential of opuntiol, isolated from Opuntia ficus-indica, against UVA radiation-mediated inflammation and skin photoaging in experimental animals. The skin-shaved experimental mouse was subjected to UVA exposure at the dosage of 10 J/cm2 per day for ten consecutive days (cumulative UVA dose: 100 J/cm2). Opuntiol (50 mg/kg b.wt.) was topically applied one hour before each UVA exposure. UVA (100 J/cm2) exposure induces epidermal hyperplasia and collagen disarrangement which leads to the photoaging-associated molecular changes in the mouse skin. Opuntiol pretreatment prevented UVA-linked clinical macroscopic skin lesions and histological changes in the mouse skin. Further, opuntiol prevents UVA-linked dermal collagen fiber loss in the mouse skin. Short-term UVA radiation (100 J/cm2) activates MAPKs through AP-1 and NF-κB p65 transcriptional pathways and subsequently induces the expression of inflammatory proteins and matrix-degrading proteinases in the mouse skin. Interestingly, opuntiol pretreatment inhibited UVA-induced activation of iNOS, VEGF, TNF-α, and COX-2 proteins and consequent activation of MMP-2, MMP-9, and MMP-12 in the mouse skin. Moreover, opuntiol was found to prevent collagen I and III breakdown in UVA radiation-exposed mouse skin. Thus, opuntiol protects mouse skin from UVA radiation-associated photoaging responses through inhibiting inflammatory responses, MAPK activation, and degradation of matrix collagen molecules.

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