scholarly journals Trehangelins ameliorate inflammation-induced skin senescence by suppressing the epidermal YAP-CCN1 axis

2021 ◽  
Author(s):  
Mami Yokota ◽  
Yoshiyuki Kamiya ◽  
Tamie Suzuki ◽  
Shinsuke Ishikawa ◽  
Akira Takeda ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Ex Vivo ◽  
Elastic Fiber ◽  
Skin Aging ◽  
Ultraviolet B ◽  
High Penetration ◽  
Extracellular Matrix Components ◽  
Cellular Communication Network ◽  
Aged Skin ◽  
Skin Explants

Abstract Trehangelins (THG) are newly identified trehalose compounds derived from broth cultures of an endophytic actinomycete, Polymorphospora rubra. THG are known to suppress Cellular Communication Network factor 1 (CCN1), which regulates collagen homeostasis in the dermis. Although the physical properties of THG suggest a high penetration of the stratum corneum, the effect of THG on the epidermis has not been reported. Here we describe a possible mechanism involved in skin aging focusing on the effect of THG on epidermal CCN1. This study shows that: 1) THG suppress epidermal CCN1 expression by inhibiting the translocation of Yes-Associated Protein (YAP) to nuclei. 2) Epidermal CCN1, localized at the basement membrane, regulates the balance between the growth and differentiation of keratinocytes. 3) Keratinocytes secrete more CCN1 than fibroblasts, which leads to disruption of the basement membrane and extracellular matrix components. 4) The secretion of CCN1 from keratinocytes is increased by ultraviolet B exposure, especially in aged keratinocytes, and deteriorates the elastic fiber structures in the underlying dermis. 5) Topical application of THG ameliorates the structure of the basement membrane in ex vivo human skin explants. Taken together, THG might be a promising treatment for aged skin by suppressing the aberrant YAP-CCN1 axis.

scholarly journals Synergistic Effect of 300 μm Needle-Depth Fractional Microneedling Radiofrequency on the Treatment of Senescence-Induced Aging Hyperpigmentation of the Skin

2021 ◽  
Vol 22 (14) ◽  
pp. 7480
Author(s):  
Young In Lee ◽  
Eunbin Kim ◽  
Dong Won Lee ◽  
Jemin Kim ◽  
Jihee Kim ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Synergistic Effect ◽  
Ex Vivo ◽  
Asian Women ◽  
Collagen Type Iv ◽  
Controlled Clinical Trial ◽  
The Novel ◽  
Type Iv ◽  
Aged Skin ◽  
Ex Vivo Study

Aging-associated dermatological pigmentary diseases are associated with accumulation of senescence cells and the disruption of basement membrane due to chronic ultraviolet radiation (UVR) exposure. Our study is on the synergistic effect of the novel 300 μm needle-depth fractional microneedling radiofrequency (FMR) treatment and conventional Q-switched ND:YAG laser on aging-associated hyperpigmentation of the skin. The prospective controlled clinical trial of 25 Asian women revealed significantly higher improvements not only on wrinkles, but also on hyperpigmentation. Additional ex vivo study revealed significant reduction of pro-melanogenic markers as well as senescent keratinocytes, while increased expression of collagen type IV on the epidermal basement membrane, after additional FMR treatment on UV-irradiated human tissues. These results demonstrate that 300 μm needle-depth FMR might effectively remove senescent keratinocytes that secrete pro-melanogenic markers, and repair disrupted basement membrane, therefore preventing constant hyperpigmentation of the aged skin.

scholarly journals Protective Effect of Spirulina-Derived C-Phycocyanin against Ultraviolet B-Induced Damage in HaCaT Cells

Medicina ◽  
2021 ◽  
Vol 57 (3) ◽  
pp. 273
Author(s):  
Young Ah Jang ◽  
Bo Ae Kim
Keyword(s):  
Antioxidant Defense System ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Control Group ◽  
Hacat Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Blue Green Algae ◽  
Radiation Group ◽  
Skin Wrinkles

Background and objectives: Reactive oxygen species (ROS) overwhelm the antioxidant defense system, induce oxidative stress, and increase matrix metalloproteinase (MMP) expression, resulting in skin aging. Thus, preventing ultraviolet B (UVB)-induced skin damage can attenuate skin aging. Spirulina (a biomass of cyanobacteria, also called blue-green algae) is comprised of prokaryotes, whereas microalgae are eukaryotes and are rich in phycocyanin, a powerful antioxidant. Materials and Methods: Here, we investigated the photoprotective effects of spirulina-derived C-phycocyanin (C-PC) against UVB radiation using keratinocytes (HaCaT cells). Results: UVB radiation increased MMP-1 and MMP-9 expression but decreased involucrin, filaggrin, and loricrin expression. C-PC showed no toxicity at concentrations of 5–80 μg/mL in terms of HaCaT cell viability. UVB-irradiated HaCaT cells had a 50.8% survival rate, which increased to 80.3% with C-PC treatment. MMP expression increased with UVB treatment, whereas MMP-1 and MMP-9 concentrations decreased with C-PC treatment. UVB reduced involucrin, filaggrin, and loricrin expression in HaCaT cells, but 80 μg/mL C-PC increased their expression by >25%. In the UVB radiation group, dichlorofluorescin diacetate fluorescence intensity in HaCaT cells increased by 81.6% compared with that in the control group, whereas ROS production was reduced by 51.2% and 55.1% upon treatment with 40 and 80 μg/mL C-PC, respectively. Conclusions: C-PC might reduce or prevent skin aging by reducing UVB irradiation-induced skin wrinkles and free radicals.

Neuropeptides and skin aging

2013 ◽  
Vol 16 (1) ◽  
Author(s):  
Rana Elewa ◽  
Evgenia Makrantonaki ◽  
Christos C. Zouboulis
Keyword(s):  
Human Skin ◽  
Inflammatory Cytokines ◽  
Vasoactive Intestinal Polypeptide ◽  
Skin Aging ◽  
Target Cells ◽  
Hormone Metabolism ◽  
Skin Cells ◽  
Calcitonin Gene ◽  
Aged Skin ◽  
Human Skin Cells

AbstractNeuropeptides (NP) are peptides that are released as chemical messengers from nerve cells. They act either in an endocrine manner, where they reach their target cells via the bloodstream or a paracrine manner, as co-transmitters modulating the function of neurotransmitters. To date approximately 100 different NP have been described in the literature. In recent years, several studies have documented that human skin expresses several functional receptors for NP, such as corticotropin-releasing hormone, melanocortins, β-endorphin, vasoactive intestinal polypeptide, neuropeptide Y and calcitonin gene-related peptide. These receptors modulate the production of inflammatory cytokines, proliferation, differentiation, lipogenesis and hormone metabolism in human skin cells. In addition, several NP are directly produced by human skin cells, indicating the complexity of understanding the real functions of NPs in human skin. In this review we address the possible effects of neuropeptides on the pathogenesis of aged skin.

scholarly journals Inflammatory Molecules Associated with Ultraviolet Radiation-Mediated Skin Aging

2021 ◽  
Vol 22 (8) ◽  
pp. 3974
Author(s):  
Tuba M. Ansary ◽  
Md. Razib Hossain ◽  
Koji Kamiya ◽  
Mayumi Komine ◽  
Mamitaro Ohtsuki
Keyword(s):  
Ultraviolet Radiation ◽  
Air Pollutants ◽  
Skin Aging ◽  
Environmental Stressors ◽  
Oxygen Species ◽  
Delayed Wound Healing ◽  
Different Types ◽  
Aged Skin ◽  
Inflammatory Molecules ◽  
Complex Organ

Skin is the largest and most complex organ in the human body comprised of multiple layers with different types of cells. Different kinds of environmental stressors, for example, ultraviolet radiation (UVR), temperature, air pollutants, smoking, and diet, accelerate skin aging by stimulating inflammatory molecules. Skin aging caused by UVR is characterized by loss of elasticity, fine lines, wrinkles, reduced epidermal and dermal components, increased epidermal permeability, delayed wound healing, and approximately 90% of skin aging. These external factors can cause aging through reactive oxygen species (ROS)-mediated inflammation, as well as aged skin is a source of circulatory inflammatory molecules which accelerate skin aging and cause aging-related diseases. This review article focuses on the inflammatory pathways associated with UVR-mediated skin aging.

Ultrasonic microrheology for ex vivo skin explants monitoring: A proof of concept

2021 ◽  
pp. 113831
Author(s):  
Vincent Gauthier ◽  
Alice Lemarquand ◽  
Emmanuel Caplain ◽  
Nicolas Wilkie-Chancellier ◽  
Stéphane Serfaty
Keyword(s):  
Ex Vivo ◽  
Proof Of Concept ◽  
Skin Explants

Abstract 5369: Mesenchymal Stem Cells Overexpressing CXCR4 (CXCR4 + -MSCs) Attenuate Remodeling of Post-Myocardial Infarction by Releasing Anti-Fibrotic Enzymes

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tao Wang ◽  
Yigang Wang ◽  
Dongsheng Zhang ◽  
Tiemin Zhao ◽  
Atif Ashraf ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Ventricular Remodeling ◽  
Interstitial Fibrosis ◽  
Ex Vivo ◽  
Genetically Engineered ◽  
Control Group ◽  
Hypoxic Conditions ◽  
Antibody Staining ◽  
Adenoviral Transduction

We hypothesize that CXCR4 + -MSCs penetrate and proliferate in infracted heart by releasing collagen degrading enzymes. We genetically engineered male mouse MSCs using ex vivo adenoviral transduction for over-expression of CXCR4/GFP or GFP alone. MSCs (G-I) or CXCR4 + -MSCs (G-II) or CXCR4 + -MSCs treated with epigallocarechin gallate (EGCG, 50μg/ml), a MT1-matrix metalloproteinases (MMPs) inhibitor (G-III) or CXCR4 + -MSCs with AMD3100 (5 μg/mL), a CXCR4-selective antagonist (G-IV). A Trans-Matrigel Chemoinvasion Assay was used to evaluate the ability of MSCs to cross the basement membrane. MMPs were analyzed by Western blot and MMP antibody staining. Sex mismatched MSCs were infused into female mice via a tail vein injection 3 days after MI. Mice in G-III were treated with EGCG (100 mg/kg, oral gavage, daily for 2 weeks) to inhibit MMPs and G-IV was treated with AMD3100 (1 mg/kg, i.p. given continually for 6 days after MI). LV fibrosis was detected by Picrosirius red staining. Echocardiography was performed at 4 weeks after MI and hearts were harvested for histological analysis. In vitro, cell migration was significantly higher in G-II in the presence of SDF-1α as compared with other groups, ( p <0.01). EGCG or AMD3100 markedly prevented this response. MMP-9 and MT1-MMP were upregulated significantly only in G-II (p<0.01) exposed to hypoxia. Infiltration of GFP and Y chromosome positive cells in the peri- or infarct area was increased significantly in G-II. CXCR4 + -MSCs penetrated more effectively into the infarcted region and survived in the ischemic environment as compared to control group. These effects were reduced with EGCG or AMD3100. The ventricular remodeling and interstitial fibrosis were also reduced in G-II but not in other groups. G-II also had less LV dilation (diastolic dimension 4.9±0.2 vs. 6.2±0.3 mm, p<0.05), EF (62±3 vs. 44±4%, p<0.05). Infarct size (31±3.8 vs 43±4.7% of LV, p<0.05) and collagen area fraction (16±2 vs. 28±4 %, p<0.05) were significantly reduced in G-2 compared to G-I. Under hypoxic conditions MMPs were upregulated in CXCR4 + -MSCs which crossed the basement membrane by releasing enzymes leading to breakdown or reduction of scar formation thus facilitating cell homing and proliferation.

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 Anti-Inflammatory and Chondroprotective Effects of Vanillic Acid and Epimedin C in Human Osteoarthritic Chondrocytes

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 932
Author(s):  
Reihane Ziadlou ◽  
Andrea Barbero ◽  
Ivan Martin ◽  
Xinluan Wang ◽  
Ling Qin ◽  
...  
Keyword(s):  
B Cells ◽  
Vanillic Acid ◽  
Ex Vivo ◽  
Cartilage Regeneration ◽  
Nuclear Factor ◽  
Treatment Groups ◽  
Extracellular Matrix Components ◽  
Gene Enhancer ◽  
Anti Inflammatory ◽  
Factor Α

In osteoarthritis (OA), inhibition of excessively expressed pro-inflammatory cytokines in the OA joint and increasing the anabolism for cartilage regeneration are necessary. In this ex-vivo study, we used an inflammatory model of human OA chondrocytes microtissues, consisting of treatment with cytokines (interleukin 1β (IL-1β)/tumor necrosis factor α (TNF-α)) with or without supplementation of six herbal compounds with previously identified chondroprotective effect. The compounds were assessed for their capacity to modulate the key catabolic and anabolic factors using several molecular analyses. We selectively investigated the mechanism of action of the two most potent compounds Vanillic acid (VA) and Epimedin C (Epi C). After identification of the anti-inflammatory and anabolic properties of VA and Epi C, the Ingenuity Pathway Analysis showed that in both treatment groups, osteoarthritic signaling pathways were inhibited. In the treatment group with VA, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling was inhibited by attenuation of the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα) phosphorylation. Epi C showed a significant anabolic effect by increasing the expression of collagenous and non-collagenous matrix proteins. In conclusion, VA, through inhibition of phosphorylation in NF-κB signaling pathway and Epi C, by increasing the expression of extracellular matrix components, showed significant anti-inflammatory and anabolic properties and might be potentially used in combination to treat or prevent joint OA.

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