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Skin Inflammation Aging and Diseases
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Skin Inflammation Aging and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 33698

Special Issue Editor

Dr. Serena Lembo

E-Mail Website
Guest Editor
Università di Salerno, Salerno, Italy
Interests: photodermatology; inflammatory skin diseases

Special Issue Information

Dear Colleagues,

The skin is the most precious dress we wear every day.

It is the body's largest organ, with a complex structure made of several tissue layers, each with a distinct cellular composition. Its most important function is to form a “barrier” to protect our body from environmental insults. The skin is a high-turnover organ, with a continuously regenerating epidermis. With aging, both the epidermis and the dermis lose their regenerative ability, undergoing thinning, wrinkling, dryness, and mottling (intrinsic aging).

The inability to restore the integrity of the skin barrier can result in many cutaneous health problems such as inflammatory skin conditions.

In turn, chronic inflammation may enhance and speed aging.

Chronic exposure to environmental elements like ultraviolet (UV) radiations cause deleterious effects in skin cells; in fact, UVA and UVB radiation are associated with skin photo-aging, various inflammatory disorders, and also skin cancer (extrinsic aging). Research in recent years has advanced our understanding of the pathophysiology of inflammatory skin diseases and skin cancer, as well as of therapeutic options for skin aging. 

Nevertheless, many aspects remain to be explored: what is the role of the skin microenvironment in aging, inflammation, and cancer? Is there a link between skin aging, chronic inflammation, and skin cancer? Do they share molecular inflammatory pathways? Can we identify predictive biomarkers?

This Special Issue calls for original research papers, full reviews, and perspectives that address our current knowledge and progress in the field of skin inflammation, aging, and disease, to find possible answers to the mentioned questions and to others related to the keywords reported below.

Dr. Serena Lembo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Skin health
  • Skin barrier
  • Inflammation Aging
  • Photoaging Intrinsic aging
  • Extrinsic aging
  • Skin cancer
  • Inflammatory skin conditions
  • Oxidative stress
  • Molecular inflammatory pathways

Published Papers (7 papers)

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Research

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13 pages, 5077 KiB  
Article
Synergistic Effect of 300 μm Needle-Depth Fractional Microneedling Radiofrequency on the Treatment of Senescence-Induced Aging Hyperpigmentation of the Skin
by Young In Lee, Eunbin Kim, Dong Won Lee, Jemin Kim, Jihee Kim, Won Jai Lee and Ju Hee Lee
Int. J. Mol. Sci. 2021, 22(14), 7480; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147480 - 13 Jul 2021
Cited by 7 | Viewed by 4925
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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18 pages, 3624 KiB  
Article
Mesenchymal Stem Cells Antagonize IFN-Induced Proinflammatory Changes and Growth Inhibition Effects via Wnt/β-Catenin and JAK/STAT Pathway in Human Outer Root Sheath Cells and Hair Follicles
by Yu-Jin Lee, Song-Hee Park, Hye-Ree Park, Young Lee, Hoon Kang and Jung-Eun Kim
Int. J. Mol. Sci. 2021, 22(9), 4581; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094581 - 27 Apr 2021
Cited by 13 | Viewed by 3078
Abstract
Mesenchymal stem cell therapy (MSCT) has been shown to be a new therapeutic option for treating alopecia areata (AA). Outer root sheath cells (ORSCs) play key roles in maintaining the hair follicle structure and supporting the bulge area. In human ORSCs (hORSCs), the [...] Read more.
Mesenchymal stem cell therapy (MSCT) has been shown to be a new therapeutic option for treating alopecia areata (AA). Outer root sheath cells (ORSCs) play key roles in maintaining the hair follicle structure and supporting the bulge area. In human ORSCs (hORSCs), the mechanism for this process has not been extensively studied. In this study, we aimed to examine the influence of human hematopoietic mesenchymal stem cells (hHMSCs) in the hORSCs in vitro model of AA and determine the mechanisms controlling efficacy. Interferon-gamma (IFN-γ) pretreatment was used to induce an in vitro model of AA in hORSCs. The effect of MSCT on the viability and migration of hORSCs was examined using co-cultures, the MTT assay, and migration assays. We investigated the expression of molecules related to the Wnt/β-catenin pathway, JAK/STAT pathway, and growth factors in hHMSC-treated hORSCs by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses. hHMSCs increased hORSC viability and migration when they were co-cultured. hHMSCs reverted IFN-γ-induced expression—including NLRP3, ASC, caspase-1, CXCL-9 through 11, IL-1β, and IL-15—and upregulated several growth factors and hair stem cell markers. hHMSCs activated several molecules in the Wnt/β-catenin signaling pathway, such as in the Wnt families, β-catenin, phosphorylated GSK-3β and cyclin D1, and suppressed the expression of DKK1 induced by IFN-γ in hORSCs. hHMSCs suppressed the phosphorylation of JAK1 to 3, STAT1, and STAT3 compared to the controls and IFN-γ-pretreated hORSCs. These results demonstrate that hHMSCs increased hORSC viability and migration in the in vitro AA model. Additionally, MSCT definitely stimulated anagen survival and hair growth in an HF organ culture model. MSCT appeared to be associated with the Wnt/β-catenin and JAK/STAT pathways in hORSCs. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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25 pages, 8426 KiB  
Article
Synthesis and Pharmacological In Vitro Investigations of Novel Shikonin Derivatives with a Special Focus on Cyclopropane Bearing Derivatives
by Nadine Kretschmer, Antje Hufner, Christin Durchschein, Katrin Popodi, Beate Rinner, Birgit Lohberger and Rudolf Bauer
Int. J. Mol. Sci. 2021, 22(5), 2774; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052774 - 09 Mar 2021
Cited by 9 | Viewed by 2627
Abstract
Melanoma is the deadliest form of skin cancer and accounts for about three quarters of all skin cancer deaths. Especially at an advanced stage, its treatment is challenging, and survival rates are very low. In previous studies, we showed that the constituents of [...] Read more.
Melanoma is the deadliest form of skin cancer and accounts for about three quarters of all skin cancer deaths. Especially at an advanced stage, its treatment is challenging, and survival rates are very low. In previous studies, we showed that the constituents of the roots of Onosma paniculata as well as a synthetic derivative of the most active constituent showed promising results in metastatic melanoma cell lines. In the current study, we address the question whether we can generate further derivatives with optimized activity by synthesis. Therefore, we prepared 31, mainly novel shikonin derivatives and screened them in different melanoma cell lines (WM9, WM164, and MUG-Mel2 cells) using the XTT viability assay. We identified (R)-1-(1,4-dihydro-5,8-dihydroxy-1,4-dioxonaphthalen-2-yl)-4-methylpent-3-enyl 2-cyclopropyl-2-oxoacetate as a novel derivative with even higher activity. Furthermore, pharmacological investigations including the ApoToxGloTM Triplex assay, LDH assay, and cell cycle measurements revealed that this compound induced apoptosis and reduced cells in the G1 phase accompanied by an increase of cells in the G2/M phase. Moreover, it showed hardly any effects on the cell membrane integrity. However, it also exhibited cytotoxicity against non-tumorigenic cells. Nevertheless, in summary, we could show that shikonin derivatives might be promising drug leads in the treatment of melanoma. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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17 pages, 4257 KiB  
Article
Ameliorating Fibrotic Phenotypes of Keloid Dermal Fibroblasts through an Epidermal Growth Factor-Mediated Extracellular Matrix Remodeling
by Hyunbum Kim, Laurensia Danis Anggradita, Sun-Jae Lee, Sung Sik Hur, Joonsuk Bae, Nathaniel Suk-Yeon Hwang, Seung Min Nam and Yongsung Hwang
Int. J. Mol. Sci. 2021, 22(4), 2198; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042198 - 23 Feb 2021
Cited by 6 | Viewed by 6279
Abstract
Keloid and hypertrophic scars are skin fibrosis-associated disorders that exhibit an uncontrollable proliferation of fibroblasts and their subsequent contribution to the excessive accumulation of extracellular matrix (ECM) in the dermis. In this study, to elucidate the underlying mechanisms, we investigated the pivotal roles [...] Read more.
Keloid and hypertrophic scars are skin fibrosis-associated disorders that exhibit an uncontrollable proliferation of fibroblasts and their subsequent contribution to the excessive accumulation of extracellular matrix (ECM) in the dermis. In this study, to elucidate the underlying mechanisms, we investigated the pivotal roles of epidermal growth factor (EGF) in modulating fibrotic phenotypes of keloid and hypertrophic dermal fibroblasts. Our initial findings revealed the molecular signatures of keloid dermal fibroblasts and showed the highest degree of skin fibrosis markers, ECM remodeling, anabolic collagen-cross-linking enzymes, such as lysyl oxidase (LOX) and four LOX-like family enzymes, migration ability, and cell–matrix traction force, at cell–matrix interfaces. Furthermore, we observed significant EGF-mediated downregulation of anabolic collagen-cross-linking enzymes, resulting in amelioration of fibrotic phenotypes and a decrease in cell motility measured according to the cell–matrix traction force. These findings offer insight into the important roles of EGF-mediated cell–matrix interactions at the cell–matrix interface, as well as ECM remodeling. Furthermore, the results suggest their contribution to the reduction of fibrotic phenotypes in keloid dermal fibroblasts, which could lead to the development of therapeutic modalities to prevent or reduce scar tissue formation. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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10 pages, 1557 KiB  
Article
Increased Histone Acetylation and Decreased Expression of Specific Histone Deacetylases in Ultraviolet-Irradiated and Intrinsically Aged Human Skin In Vivo
by Yuri Lee, Mi Hee Shin, Min-Kyoung Kim, Yeon Kyung Kim, Hye Sun Shin, Dong Hun Lee and Jin Ho Chung
Int. J. Mol. Sci. 2021, 22(4), 2032; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042032 - 18 Feb 2021
Cited by 13 | Viewed by 3844
Abstract
Histone deacetylases (HDACs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins and play a crucial role in epigenetic regulation. Previously, we showed that histone acetylation is implicated in ultraviolet (UV)-induced inflammation and matrix impairment. To [...] Read more.
Histone deacetylases (HDACs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins and play a crucial role in epigenetic regulation. Previously, we showed that histone acetylation is implicated in ultraviolet (UV)-induced inflammation and matrix impairment. To elucidate the histone acetylation status and specific HDACs involved in skin aging, we examined the changes in histone acetylation, global HDAC activity, and the expression of HDACs and sirtuins (SIRTs) in intrinsically aged and photoaged human skin as well as in UV-irradiated human skin in vivo. Following acute UV irradiation, the acetylated histone H3 (AcH3) level was increased, but HDAC activity and the expression levels of HDAC4, HDAC11, and SIRT4 were significantly decreased. In intrinsically aged skin, AcH3 levels were increased, but HDAC activity and the expression levels of HDAC4, HDAC5, HDAC10, HDAC11, SIRT6, and SIRT7 were significantly decreased. However, histone acetylation and HDAC expression in photoaged skin were not significantly different from those in intrinsically aged skin. Collectively, HDAC4 and HDAC11 were decreased in both UV-irradiated and intrinsically aged skin, suggesting that they may play a universal role in increased histone acetylation associated with skin aging. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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10 pages, 2157 KiB  
Article
UV-Induced Reduction of ACVR1C Decreases SREBP1 and ACC Expression by the Suppression of SMAD2 Phosphorylation in Normal Human Epidermal Keratinocytes
by Yu-Dan Tian, Min Hwa Chung, Qing-Ling Quan, Dong Hun Lee, Eun Ju Kim and Jin Ho Chung
Int. J. Mol. Sci. 2021, 22(3), 1101; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031101 - 22 Jan 2021
Cited by 2 | Viewed by 2350
Abstract
Activin A receptor type 1C (ACVR1C), a type I transforming growth factor-β (TGF-β) receptor, has been implicated in sensitive skin and psoriasis and is involved in the regulation of metabolic homeostasis as well as cell proliferation and differentiation. In this study, we identified [...] Read more.
Activin A receptor type 1C (ACVR1C), a type I transforming growth factor-β (TGF-β) receptor, has been implicated in sensitive skin and psoriasis and is involved in the regulation of metabolic homeostasis as well as cell proliferation and differentiation. In this study, we identified a novel role of ACVR1C in the ultraviolet (UV)-irradiation-induced reduction of epidermal lipogenesis in human skin. UV irradiation decreased ACVR1C expression and epidermal triglyceride (TG) synthesis in human skin in vivo and in primary normal human epidermal keratinocytes (NHEK) in vitro. Lipogenic genes, including genes encoding acetyl-CoA carboxylase (ACC) and sterol regulatory element binding protein-1 (SREBP1), were significantly downregulated in UV-irradiated NHEK. ACVR1C knockdown by shRNA resulted in greater decreases in SREBP1 and ACC in response to UV irradiation. Conversely, the overexpression of ACVR1C attenuated the UV-induced decreases in SREBP1 and ACC. Further mechanistic study revealed that SMAD2 phosphorylation mediated the ACVR1C-induced lipogenic gene modulation. Taken together, a decrease in ACVR1C may cause UV-induced reductions in SREBP1 and ACC as well as epidermal TG synthesis via the suppression of SMAD2 phosphorylation. ACVR1C may be a target for preventing or treating UV-induced disruptions in lipid metabolism and associated skin disorders. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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Review

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13 pages, 885 KiB  
Review
Cellular Senescence and Inflammaging in the Skin Microenvironment
by Young In Lee, Sooyeon Choi, Won Seok Roh, Ju Hee Lee and Tae-Gyun Kim
Int. J. Mol. Sci. 2021, 22(8), 3849; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083849 - 08 Apr 2021
Cited by 74 | Viewed by 9509
Abstract
Cellular senescence and aging result in a reduced ability to manage persistent types of inflammation. Thus, the chronic low-level inflammation associated with aging phenotype is called “inflammaging”. Inflammaging is not only related with age-associated chronic systemic diseases such as cardiovascular disease and diabetes, [...] Read more.
Cellular senescence and aging result in a reduced ability to manage persistent types of inflammation. Thus, the chronic low-level inflammation associated with aging phenotype is called “inflammaging”. Inflammaging is not only related with age-associated chronic systemic diseases such as cardiovascular disease and diabetes, but also skin aging. As the largest organ of the body, skin is continuously exposed to external stressors such as UV radiation, air particulate matter, and human microbiome. In this review article, we present mechanisms for accumulation of senescence cells in different compartments of the skin based on cell types, and their association with skin resident immune cells to describe changes in cutaneous immunity during the aging process. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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