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Special Issue "Skin Histopathology: Focused on Ageing and Cancer"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 6518

Special Issue Editors

Dr. Lukas Lacina
E-Mail Website
Guest Editor
Dpt. of Dermatovenerology, First Faculty of Medicine, Charles University, U nemocnice 2, 128 00 Praha 2, Czech Republic
Interests: skin; cancer; skin disease; cell biology
Special Issues, Collections and Topics in MDPI journals
Dr. Michal Kolář
E-Mail Website1 Website2
Guest Editor
Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
Interests: genetics; genomics; transcriptomics; epigenetics; molecular biology; cancer; development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skin represents the largest organ of the human body with numerous physiological functions. Notably, the skin as a barrier is life-long exposed to the outer environment, and it is facing all its potentially damaging effects. Therefore human skin suffers from both either intrinsic ageing, but also extrinsic factors enhancing this process.

Ageing is accompanied by a plethora of phenotypic changes in the structure of cutaneous cells and extracellular matrix, but also by their functional changes.  As a result, aged skin is associated with higher susceptibility to poor self-renewal and healing, with increased risk of development of various dermatoses, and it is also prone to develop skin cancer.

In this Special Issue, we wish to broaden our understanding to skin ageing, highlight recent hot topics in structural and functional changes of skin and also unveil molecular mechanisms leading to these changes.

We aim to promote knowledge and understanding of the various facets related to skin health and disease with emphasis on various aspects of cutaneous ageing-related pathologies because it can strengthen our diagnostic and treatment strategies and potentially prevent or even reverse skin ageing.

Dr. Lukas Lacina
Dr. Michal Kolář
Guest Editors

Manuscript Submission Information

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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

  • epidermis
  • dermis
  • senescence-associated secretory phenotype
  • ageing
  • dermatoporosis
  • healing
  • cancer
  • photodamage
  • stem cell
  • renewal

Published Papers (5 papers)

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Research

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Article
The Beneficial Effect of Rosmarinic Acid on Benzophenone-3-Induced Alterations in Human Skin Fibroblasts
Int. J. Mol. Sci. 2021, 22(21), 11451; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111451 - 23 Oct 2021
Viewed by 628
Abstract
Benzophenone-3 (BP-3) is one of the most widely used chemical sunscreens. The results of many in vitro and in vivo tests confirm its high percutaneous penetration and systemic absorption, which question the safety of its wide use. The aim of our research was [...] Read more.
Benzophenone-3 (BP-3) is one of the most widely used chemical sunscreens. The results of many in vitro and in vivo tests confirm its high percutaneous penetration and systemic absorption, which question the safety of its wide use. The aim of our research was to assess the effect of this compound on components of the skin extracellular matrix, and to investigate whether rosmarinic acid (RA) could reduce BP-3-induced changes in human skin fibroblasts. BP-3 used at concentrations of 0.1–100 µM caused a number of unfavorable changes in the level of type I collagen, decorin, sulfated glycosaminoglycans, hyaluronic acid, elastin, and expression or activity of matrix metalloproteinases (MMP-1, MMP-2), elastase and hyaluronidase. Moreover, the intracellular retention of collagen was accompanied by changes in the expression of proteins modifying and controlling the synthesis and secretion of this protein. Most importantly, RA at a concentration of 100 µM significantly reduced or completely abolished the adverse effects of BP-3. Based on these findings, it can be concluded that this polyphenol may provide effective protection against BP-3-induced disturbances in skin cells, which may have important clinical implications. Full article
(This article belongs to the Special Issue Skin Histopathology: Focused on Ageing and Cancer)
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Article
AP Collagen Peptides Prevent Cortisol-Induced Decrease of Collagen Type I in Human Dermal Fibroblasts
Int. J. Mol. Sci. 2021, 22(9), 4788; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094788 - 30 Apr 2021
Viewed by 1522
Abstract
Cortisol is an endogenous glucocorticoid (GC) and primary stress hormone that regulates a wide range of stress responses in humans. The adverse effects of cortisol on the skin have been extensively documented but the underlying mechanism of cortisol-induced signaling is still unclear. In [...] Read more.
Cortisol is an endogenous glucocorticoid (GC) and primary stress hormone that regulates a wide range of stress responses in humans. The adverse effects of cortisol on the skin have been extensively documented but the underlying mechanism of cortisol-induced signaling is still unclear. In the present study, we investigate the effect of cortisol on collagen type I expression and the effect of AP collagen peptides, collagen tripeptide-rich hydrolysates containing 3% glycine-proline- hydroxyproline (Gly-Pro-Hyp, GPH) from the fish skin, on the cortisol-mediated inhibition of collagen type I and the cortisol-induced signaling that regulates collagen type I production in human dermal fibroblasts (HDFs). We determine that cortisol downregulates the expression of collagen type I. AP collagen peptides or GC receptor (GR) inhibitors recover the cortisol-mediated inhibition of collagen type I and GR activation. AP collagen peptides or GR inhibitors also prevent the cortisol-dependent inhibition of transforming growth factor (TGF)-β signaling. AP collagen peptides or GR inhibitors are effective in the prevention of collagen type I inhibition mediated by cortisol in senescent HDFs and reconstituted human skin models. Taken together, GR signaling might be responsible for the cortisol-mediated inhibition of TGF-β. AP collagen peptides act as GR-mediated signaling blockers, preventing the cortisol-dependent inhibition of collagen type I. Therefore, AP collagen peptides have the potential to improve skin health. Full article
(This article belongs to the Special Issue Skin Histopathology: Focused on Ageing and Cancer)
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Review

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Review
Cancer-Associated Fibroblasts Influence the Biological Properties of Malignant Tumours via Paracrine Secretion and Exosome Production
Int. J. Mol. Sci. 2022, 23(2), 964; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020964 - 16 Jan 2022
Cited by 2 | Viewed by 992
Abstract
Cancer-associated fibroblasts (CAFs) are an essential component of the tumour microenvironment. They represent a heterogeneous group of cells that are under the control of cancer cells and can reversely influence the cancer cell population. They affect the cancer cell differentiation status, and the [...] Read more.
Cancer-associated fibroblasts (CAFs) are an essential component of the tumour microenvironment. They represent a heterogeneous group of cells that are under the control of cancer cells and can reversely influence the cancer cell population. They affect the cancer cell differentiation status, and the migration and formation of metastases. This is achieved through the production of the extracellular matrix and numerous bioactive factors. IL-6 seems to play the central role in the communication of noncancerous and cancer cells in the tumour. This review outlines the role of exosomes in cancer cells and cancer-associated fibroblasts. Available data on the exosomal cargo, which can significantly intensify interactions in the tumour, are summarised. The role of exosomes as mediators of the dialogue between cancer cells and cancer-associated fibroblasts is discussed together with their therapeutic relevance. The functional unity of the paracrine- and exosome-mediated communication of cancer cells with the tumour microenvironment represented by CAFs is worthy of attention. Full article
(This article belongs to the Special Issue Skin Histopathology: Focused on Ageing and Cancer)
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Review
Structural and Functional Changes and Possible Molecular Mechanisms in Aged Skin
Int. J. Mol. Sci. 2021, 22(22), 12489; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212489 - 19 Nov 2021
Cited by 1 | Viewed by 1072
Abstract
Skin aging is a complex process influenced by intrinsic and extrinsic factors. Together, these factors affect the structure and function of the epidermis and dermis. Histologically, aging skin typically shows epidermal atrophy due to decreased cell numbers. The dermis of aged skin shows [...] Read more.
Skin aging is a complex process influenced by intrinsic and extrinsic factors. Together, these factors affect the structure and function of the epidermis and dermis. Histologically, aging skin typically shows epidermal atrophy due to decreased cell numbers. The dermis of aged skin shows decreased numbers of mast cells and fibroblasts. Fibroblast senescence contributes to skin aging by secreting a senescence-associated secretory phenotype, which decreases proliferation by impairing the release of essential growth factors and enhancing degradation of the extracellular matrix through activation of matrix metalloproteinases (MMPs). Several molecular mechanisms affect skin aging including telomere shortening, oxidative stress and MMP, cytokines, autophagic control, microRNAs, and the microbiome. Accumulating evidence on the molecular mechanisms of skin aging has provided clinicians with a wide range of therapeutic targets for treating aging skin. Full article
(This article belongs to the Special Issue Skin Histopathology: Focused on Ageing and Cancer)
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Review
Impaired Wound Healing, Fibrosis, and Cancer: The Paradigm of Recessive Dystrophic Epidermolysis Bullosa
Int. J. Mol. Sci. 2021, 22(10), 5104; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105104 - 12 May 2021
Cited by 5 | Viewed by 1490
Abstract
Recessive Dystrophic Epidermolysis Bullosa (RDEB) is a devastating skin blistering disease caused by mutations in the gene encoding type VII collagen (C7), leading to epidermal fragility, trauma-induced blistering, and long term, hard-to-heal wounds. Fibrosis develops rapidly in RDEB skin and contributes to both [...] Read more.
Recessive Dystrophic Epidermolysis Bullosa (RDEB) is a devastating skin blistering disease caused by mutations in the gene encoding type VII collagen (C7), leading to epidermal fragility, trauma-induced blistering, and long term, hard-to-heal wounds. Fibrosis develops rapidly in RDEB skin and contributes to both chronic wounds, which emerge after cycles of repetitive wound and scar formation, and squamous cell carcinoma—the single biggest cause of death in this patient group. The molecular pathways disrupted in a broad spectrum of fibrotic disease are also disrupted in RDEB, and squamous cell carcinomas arising in RDEB are thus far molecularly indistinct from other sub-types of aggressive squamous cell carcinoma (SCC). Collectively these data demonstrate RDEB is a model for understanding the molecular basis of both fibrosis and rapidly developing aggressive cancer. A number of studies have shown that RDEB pathogenesis is driven by a radical change in extracellular matrix (ECM) composition and increased transforming growth factor-beta (TGFβ) signaling that is a direct result of C7 loss-of-function in dermal fibroblasts. However, the exact mechanism of how C7 loss results in extensive fibrosis is unclear, particularly how TGFβ signaling is activated and then sustained through complex networks of cell-cell interaction not limited to the traditional fibrotic protagonist, the dermal fibroblast. Continued study of this rare disease will likely yield paradigms relevant to more common pathologies. Full article
(This article belongs to the Special Issue Skin Histopathology: Focused on Ageing and Cancer)
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