Objective: RIS-1/psoriasin/S100A7 is an epithelial antimicrobial peptide, whose expression is upregulated in inflammatory skin diseases and is induced by retinoids. Its molecular expression was investigated in skin cell cultures and in skin specimens to better understand its role in inflammatory procedures of the pilosebaceous unit.
Methods: rtPCR and northern blotting of RIS-1/psoriasin and the retinoid-metabolizing genes CYP26AI and CRABP-II were performed in cells cultures (keratinocytes, sebocytes, fibroblasts, endothelial cells, melanocytes, lymphocytes and prostate cells; native and treated with retinoids) and in situ hybridization in normal and inflamed skin (acne, psoriasis).
Results: a) RIS-1/psoriasin is expressed in keratinocytes and fibroblasts and in keratinocytes of the stratum granulosum . Retinoids and inflammatory conditions increase the levels of RIS-1/psoriasin in keratinocytes (both), sebocytes (inflammation only) and fibroblasts (retinoids). Sebocytes and fibroblasts are the metabolically most active skin cells, since they can upregulate the expression of CRABP-II and CYP26AI, genes responsible for retinoid metabolism. Inflammation modifies the compartmentation of RIS-1/psoriasin in sebaceous glands and the follicular root sheaths.
Conclusion: The present data indicate that anti-inflammatory treatment targeting the epithelial compartments of the skin, including such with antibacterial peptides, may be promising for inflammatory skin diseases.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5821165 | PMC |
http://dx.doi.org/10.1080/19381980.2017.1338993 | DOI Listing |
Arch Dermatol Res
January 2025
Department of Dermatology, Medical Research and Clinical Studies Institute, National Research Centre, Giza, Egypt.
Acne vulgaris is a common and challenging condition to treat. To assess the effect of botulinum toxin type A (BTX-A) in the treatment of mild to moderate acne vulgaris. This study included 30 patients with mild to moderate acne vulgaris treated with intradermal injections of diluted BTX-A (microbotox) on the cheek in a regular grid pattern using very small droplets (microbotox).
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Dermatology and Venereology Department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt.
Morphea is a chronic inflammatory fibrosing disorder. Since fibrosis is the hallmark of both scars and morphea, our attention was raised for the possible use of Fractional Ablative CO lasers and microneedling as treatment modalities for morphea. To compare the efficacy and safety of Fractional Ablative CO lasers and microneedling in the treatment of morphea.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Genetics & Biotechnology, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Youngin, 17104, Republic of Korea.
Abnormal melanin synthesis within melanocytes can result in pigmentary skin disorders. Although pigmentation alterations associated with inflammation are frequently observed, the precise reason for this clinical observation is still unknown. More specifically, although many cytokines are known to be critical for inflammatory skin processes, it is unclear how they affect epidermal melanocyte function.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Dermatology, Faculty of Medicine, Fayoum University, Fayoum, Egypt.
Vitiligo is considered as depigmenting skin disorder where patches of skin losing their pigment. Lipocalin-2 (LCN2) is one of the Inflammatory adipokines that has a potential role in skin disorders and other inflammatory diseases as well. To measure the concentration level of LCN2 in vitiligo patients compared to healthy controls and to investigate its relation to disease activity and other clinical data to evaluate its role in the pathogenesis of the disease.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
We have recently shown that fluoxetine (FX) suppressed polyinosinic-polycytidylic acid-induced inflammatory response and endothelin release in human epidermal keratinocytes, via the indirect inhibition of the phosphoinositide 3-kinase (PI3K)-pathway. Because PI3K-signaling is a positive regulator of the proliferation, in the current, highly focused follow-up study, we assessed the effects of FX (14 µM) on the proliferation and differentiation of human epidermal keratinocytes. We found that FX exerted anti-proliferative actions in 2D cultures (HaCaT and primary human epidermal keratinocytes [NHEKs]; 48- and 72-h; CyQUANT-assay) as well as in 3D reconstructed epidermal equivalents (48-h; Ki-67 immunohistochemistry).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!