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Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0
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Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0

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: 30 April 2024 | Viewed by 6575

Special Issue Editors

Dr. Paola Maura Ticarico

E-Mail Website
Guest Editor
Institute for Maternal and Child Health - IRCCS “Burlo Garofolo”, Via dell’Istria 65/1, 34137 Trieste, Italy
Interests: cell biology; apoptosis; keratinocytes; keratinocytes differentiation; keratinocytes proliferation; notch signaling; dermatology diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Sergio Crovella

E-Mail Website
Co-Guest Editor
1. Institute for Maternal and Child Health—IRCCS “Burlo Garofolo”, 34137 Trieste, Italy
2. Department of Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Doha, Qatar
Interests: immunology; clinical pathology; molecular genetics; molecular biology; OMICs; bioinformatics
Special Issues, Collections and Topics in MDPI journals
Dr. Luisa Zupin

E-Mail Website
Co-Guest Editor
Department of Medical Genetics, IRCCS Ospedale Infantile Burlo Garofolo, Trieste, Italy
Interests: photobiomodulation therapy; skin disorder
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In addition to providing physical, chemical, and biological protection against the external environment, the skin barrier is important for maintaining homeostasis by preventing an excessive loss of water, ions, and serum proteins.

Keratinocytes are the main cell type of the epidermis and originate in the basal layer, in which keratinocytes are mitotically active; then, they progressively differentiate and migrate upwards to the stratum corneum. In keratinocytes, cell–cell adhesions are necessary for structural integrity and barrier formation of the epidermis. Moreover, keratinocytes actively contribute to the cutaneous immune responses, producing a plethora of inflammatory mediators.

Defects in keratinocytes differentiation, proliferation, cell–cell junction, and inflammation are closely related to many inflammatory skin diseases, such as hidradenitis suppurativa, psoriasis, atopic dermatitis, and Behçet disease.

This Special Issue is dedicated to the role of keratinocytes in skin diseases. Areas of particular interest include but are not limited to keratinization and skin diseases, autoinflammatory keratinization diseases, and Notch signaling regulation in skin diseases.

Dr. Paola Maura Ticarico
Prof. Dr. Sergio Crovella
Dr. Luisa Zupin
Guest Editors

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

  • dermatological diseases
  • keratinocytes
  • cell–cell junction
  • inflammation
  • autoinflammation
  • differentiation
  • keratinization
  • proliferation
  • treatment

Published Papers (4 papers)

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Research

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13 pages, 3364 KiB  
Article
Inhibition of NLRP3 Inflammasome Activation by 3H-1,2-Dithiole-3-Thione: A Potential Therapeutic Approach for Psoriasis Treatment
by Meng-Chieh Shih, Chia-Ling Li, En-Chih Liao, Chung-Yang Yen, Ling-Jung Yen, Kai-Chun Wang, Ling-Ying Lu, Ting-Yu Chou, Ying-Chin Chen and Sheng-Jie Yu
Int. J. Mol. Sci. 2023, 24(17), 13528; https://doi.org/10.3390/ijms241713528 - 31 Aug 2023
Cited by 1 | Viewed by 1028
Abstract
Psoriasis is a chronic autoimmune skin disease with a significant impact on quality of life and potential for severe comorbidities. Inflammation in the skin is induced by immune cells that overexpress pro-inflammatory cytokines, with the Th17 cell playing a crucial role. NLRP3 inflammasome [...] Read more.
Psoriasis is a chronic autoimmune skin disease with a significant impact on quality of life and potential for severe comorbidities. Inflammation in the skin is induced by immune cells that overexpress pro-inflammatory cytokines, with the Th17 cell playing a crucial role. NLRP3 inflammasome activation is associated with inflammatory diseases and abnormal T cell differentiation. 3H-1,2-dithiole-3-thione (D3T), isolated from cruciferous vegetables, has anti-inflammatory effects and inhibits Th17 differentiation. This study aimed to investigate how D3T reduces skin inflammation and modulates Th17 cell differentiation by inhibiting NLRP3 inflammasome activation. In an imiquimod-induced psoriasis mouse model, D3T treatment demonstrated significant reductions in ear thickness, skin redness, and scaling compared to a control group. Our study also observed decreased expression of ki-67, NLRP3 inflammasome, and cleaved caspase-1 in skin samples, reduced levels of IL-6 and IL-17A in serum samples, and inhibition of Th17 differentiation after D3T application. D3T could also inhibit the expression of NLRP3, caspase-1, and IL-1β in TNF-α stimulated HaCaT cells. The mechanical study also revealed that D3T could inhibit NLRP3 inflammasome activation by inhibiting the JNK pathway in HaCaT cells. These results indicate that targeting NLRP3 inflammasome activation is a promising strategy in the treatment of psoriasis. Full article
(This article belongs to the Special Issue Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0)
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16 pages, 6157 KiB  
Article
Epidermal Loss of RORα Enhances Skin Inflammation in a MC903-Induced Mouse Model of Atopic Dermatitis
by Xiangmei Hua, Conrad Dean Blosch, Hannah Dorsey, Maria K. Ficaro, Nicole L. Wallace, Richard P. Hsung and Jun Dai
Int. J. Mol. Sci. 2023, 24(12), 10241; https://doi.org/10.3390/ijms241210241 - 16 Jun 2023
Viewed by 2352
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease featuring skin barrier dysfunction and immune dysregulation. Previously, we reported that the retinoid-related orphan nuclear receptor RORα was highly expressed in the epidermis of normal skin. We also found that it positively regulated the [...] Read more.
Atopic dermatitis (AD) is a chronic inflammatory skin disease featuring skin barrier dysfunction and immune dysregulation. Previously, we reported that the retinoid-related orphan nuclear receptor RORα was highly expressed in the epidermis of normal skin. We also found that it positively regulated the expression of differentiation markers and skin barrier-related genes in human keratinocytes. In contrast, epidermal RORα expression was downregulated in the skin lesions of several inflammatory skin diseases, including AD. In this study, we generated mouse strains with epidermis-specific Rora ablation to understand the roles of epidermal RORα in regulating AD pathogenesis. Although Rora deficiency did not cause overt macroscopic skin abnormalities at the steady state, it greatly amplified MC903-elicited AD-like symptoms by intensifying skin scaliness, increasing epidermal hyperproliferation and barrier impairment, and elevating dermal immune infiltrates, proinflammatory cytokines, and chemokines. Despite the normal appearance at the steady state, Rora-deficient skin showed microscopic abnormalities, including mild epidermal hyperplasia, increased TEWL, and elevated mRNA expression of Krt16, Sprr2a, and Tslp genes, indicating subclinical impairment of epidermal barrier functions. Our results substantiate the importance of epidermal RORα in partially suppressing AD development by maintaining normal keratinocyte differentiation and skin barrier function. Full article
(This article belongs to the Special Issue Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0)
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Review

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17 pages, 1037 KiB  
Review
Key Factors in the Complex and Coordinated Network of Skin Keratinization: Their Significance and Involvement in Common Skin Conditions
by Nives Pondeljak, Liborija Lugović-Mihić, Lucija Tomić, Ena Parać, Lovre Pedić and Elvira Lazić-Mosler
Int. J. Mol. Sci. 2024, 25(1), 236; https://doi.org/10.3390/ijms25010236 - 23 Dec 2023
Viewed by 935
Abstract
The epidermis serves many vital roles, including protecting the body from external influences and healing eventual injuries. It is maintained by an incredibly complex and perfectly coordinated keratinization process. In this process, desquamation is essential for the differentiation of epidermal basal progenitor cells [...] Read more.
The epidermis serves many vital roles, including protecting the body from external influences and healing eventual injuries. It is maintained by an incredibly complex and perfectly coordinated keratinization process. In this process, desquamation is essential for the differentiation of epidermal basal progenitor cells into enucleated corneocytes, which subsequently desquamate through programmed death. Numerous factors control keratinocyte differentiation: epidermal growth factor, transforming growth factor-α, keratinocyte growth factor, interleukins IL-1-β and IL-6, elevated vitamin A levels, and changes in Ca2+ concentration. The backbone of the keratinocyte transformation process from mitotically active basal cells into fully differentiated, enucleated corneocytes is the expression of specific proteins and the creation of a Ca2+ and pH gradient at precise locations within the epidermis. Skin keratinization disorders (histologically characterized predominantly by dyskeratosis, parakeratosis, and hyperkeratosis) may be categorized into three groups: defects in the α-helical rod pattern, defects outside the α-helical rod domain, and disorders of keratin-associated proteins. Understanding the process of keratinization is essential for the pathogenesis of many dermatological diseases because improper desquamation and epidermopoiesis/keratinization (due to genetic mutations of factors or due to immune pathological processes) can lead to various conditions (ichthyoses, palmoplantar keratodermas, psoriasis, pityriasis rubra pilaris, epidermolytic hyperkeratosis, and others). Full article
(This article belongs to the Special Issue Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0)
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27 pages, 1311 KiB  
Review
Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling
by Liam E. Carman, Michael L. Samulevich and Brian J. Aneskievich
Int. J. Mol. Sci. 2023, 24(15), 11943; https://doi.org/10.3390/ijms241511943 - 26 Jul 2023
Viewed by 1354
Abstract
The overactivity of keratinocyte cytoplasmic signaling contributes to several cutaneous inflammatory and immune pathologies. An important emerging complement to proteins responsible for this overactivity is signal repression brought about by several proteins and protein complexes with the native role of limiting inflammation. The [...] Read more.
The overactivity of keratinocyte cytoplasmic signaling contributes to several cutaneous inflammatory and immune pathologies. An important emerging complement to proteins responsible for this overactivity is signal repression brought about by several proteins and protein complexes with the native role of limiting inflammation. The signaling repression by these proteins distinguishes them from transmembrane receptors, kinases, and inflammasomes, which drive inflammation. For these proteins, defects or deficiencies, whether naturally arising or in experimentally engineered skin inflammation models, have clearly linked them to maintaining keratinocytes in a non-activated state or returning cells to a post-inflamed state after a signaling event. Thus, together, these proteins help to resolve acute inflammatory responses or limit the development of chronic cutaneous inflammatory disease. We present here an integrated set of demonstrated or potentially inflammation-repressive proteins or protein complexes (linear ubiquitin chain assembly complex [LUBAC], cylindromatosis lysine 63 deubiquitinase [CYLD], tumor necrosis factor alpha-induced protein 3-interacting protein 1 [TNIP1], A20, and OTULIN) for a comprehensive view of cytoplasmic signaling highlighting protein players repressing inflammation as the needed counterpoints to signal activators and amplifiers. Ebb and flow of players on both sides of this inflammation equation would be of physiological advantage to allow acute response to damage or pathogens and yet guard against chronic inflammatory disease. Further investigation of the players responsible for repressing cytoplasmic signaling would be foundational to developing new chemical-entity pharmacologics to stabilize or enhance their function when clinical intervention is needed to restore balance. Full article
(This article belongs to the Special Issue Functional Defects of Keratinocytes in Inflammatory Skin Diseases 2.0)
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