Advanced Glycation Endproducts in Aging Skin
Sara C. Zapico in Mechanisms Linking Aging, Diseases and Biological Age Estimation, 2017
As glycation is a slow procedure, accumulation of AGEs is mainly dependent on protein turnover rate. Therefore, dermal long-lived proteins like collagens type I and IV and fibronectin represent the major targets of AGE-modification (Verzijl et al. 2000, Dyer et al. 1993). Specifically, the appearance of glycated collagen is being first observed in the age of 20. With an accumulation rate of about 3.7% per year, it reaches 30–50% at 80 years of age (Dunn et al. 1991). Recently, N-ε-CML was detected in keratin 10 in the epidermis of healthy donors, pointing to a potential role of more short-lived proteins in glycation processes (Kawabata et al. 2011). Accordingly, in an in vitro reconstructed organ skin model, both epidermis and dermis were modified by glycation (Pageon et al. 2008).
Chronic Otitis Media
John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed in Paediatrics, The Ear, Skull Base, 2018
Recently, Yamamoto-Fukuda et al. 62 performed an elegant study using a hybrid gerbil model to demonstrate that the epithelial cells in cholesteatoma are derived from the tympanic membrane and not from the epithelial cells within the middle ear or epithelium from the external auditory canal. Indeed, the molecular pathology of cholesteatoma has been investigated by a number of authors. Using DNA chip analysis, 282 genes were found to be differentially expressed in comparison to the control samples63 and Klenke et al. 64 identified 3558 new cholesteatoma-related transcripts. Of those, 811 were upregulated and 334 downregulated more than twofold. The genes involved are found in a number of different biological processes including signal transduction, cell growth, cell communication, metabolism, transport and the immune response. Hamajima et al. 65 determined the role of inhibitor of DNA-binding (Id1) in the proliferation of cholesteatoma keratinocytes. They found that Id1, a protein that leads to cell immortalization, induces up regulation of NF-ºB/cyclin D1/keratin 10 in the keratinocytes. The authors concluded that Id1 contributed to the thickening of the middle ear mucosa, cell cycle progression and removal of cell cycle inhibition.
Endocrine and Metabolic Side Effects
Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish in Retinoids in Dermatology, 2019
Daily oral application of 30 mg alitretinoin in patients with chronic hand eczema increased Ki-67-positive cells in the suprabasal layer and a normalized dysregulated expression of various skin barrier genes (claudin 1, loricrin, filaggrin, and cytokeratin 10) and TSLP (175). Alitretinoin is also negative regulator of TSLP expression in airway epithelial cells (176). Inhibition of IL-1β-dependent genes by active RXRs involves antagonism of NF-κB signaling (177).
Portulaca oleracea extract relieves skin barrier damage induced by increased photosensitivity after GA peeling
Published in Cutaneous and Ocular Toxicology, 2022
Jing Wei, Qianghua Quan, Peiyu Wang, Yiming Wang, Tong Huo, Quan An
Modern studies have revealed that P. oleracea extract is capable of regulating the TNF-α-induced NF-κB signalling pathway as well as suppressing the overexpression of pro-inflammatory factors25. Zhao et al.26 reported that with the use of a cream containing calcipotriol ointment and P. oleracea extract for four consecutive weeks, the protein expression levels of Keratin 10 (K10), loricrin (LOR), and FLG were significantly downregulated in psoriatic lesions and TEWL values were significantly decreased. Keratins are the major proteins in the epidermis. They build the intermediate filament (IF) cytoskeleton, which provides epidermal stability because they are highly crosslinked with the cornified envelope. Keratin 1 (K1) and K10 are among the first keratins to be expressed during cornification27. LOR is synthesized and subsequently crosslinked by several transglutaminases to reinforce epidermal stability28. These studies have shown that P. oleracea has effects on inhibiting inflammation and repairing the skin barrier. Our research also confirmed that P. oleracea can relieve damage to the skin barrier and inflammation induced by GA + UVB.
Protective mechanism of GPR30 agonist G1 against ultraviolet B-induced injury in epidermal stem cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Yaqin Zhang, Li Li, Yangchun Xu, Xiaoli Zhao, Fuqiu Li
ESCs were isolated from the skin on the backs of 8-week-old C57BL/6 mice. Briefly, the mouse skin was dissected and placed in HBSS and minced into small pieces. The tissues were then digested with 0.25% trypsin and vortexed several times to ensure adequate mixing. The digested cells were then spun to remove the supernatant, and the pellets were suspended and seeded into a six-well culture plate in DMEM/F12 medium containing 4 ng/ml bFGF (Thermo Fisher Scientific, Waltham, MA). To identify ESCs, isolated cells were detected using a flow cytometer (Thermo Fisher Scientific, Waltham, MA) with following antibodies: integrin β1 (ab179471, Abcam, Cambridge, UK), keratin 19 (ab191208, Abcam, Cambridge, UK) and keratin 10 (ab76318, Abcam, Cambridge, UK) using a method as previously reported [12,13]. The percentages of integrin β1- and KRT19-positive cells were greater than 85%, and the percentage of KRT10-positive cells was lesser than 10%. The ESCs were passaged every 3–5 days and used for low passage numbers. ESCs were stimulated with ultraviolet B (UV-B) (50 mJ/cm2) with or without 7.5 and 15 μM G1 [14] for 24 h.
The most promising microneedle device: present and future of hyaluronic acid microneedle patch
Published in Drug Delivery, 2022
Huizhi Kang, Zhuo Zuo, Ru Lin, Muzi Yao, Yang Han, Jing Han
In addition, HA-CD44 interaction (Figure 5) also affects epidermal structure and function by upregulating the expression of differentiation markers (e.g., involucrin [IVL], profilaggrin, and keratin 10 [K-10]) to trigger proliferation and differentiation of keratin-forming cells and regulating lipid synthesis or secretion, thereby affecting the homeostasis of the permeability barrier (Bourguignon et al., 2006).
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