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The Ichthyosis (ic) Mutation, Chromosome 1
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
John P. Sundberg, Mark R. Pittelkow
The chromosomal location of trichothiodystrophy has not been mapped, but a group of differentiation-related gene products, including trichohyalin, profilaggrin, involucrin, loricrin, psoriasin, CRABP-II, and MRP 8 and 14 map to human Chromosome lq21,20 and the mouse ichthyosis mutation, located on Chromosome 1, may have homology within these loci.
Mechanism of Action of Topical Retinoids
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Sümeyre Seda Ertekin, Mehmet Salih Gurel
Tazarotene is a prodrug that undergoes esterase hydrolysis in cutaneous tissue to form its active metabolite, tazarotenic acid. It has a higher affinity to RAR-γ/β than RAR-α, but it does not bind to RXR (3). Its FDA-approved indications for topical use are psoriasis and acne vulgaris. It modulates the pathogenesis of psoriasis by regulating gene expression of retinoid-induced genes, including those that regulate cell proliferation, differentiation, and inflammation. Tazarotene appears to downregulate the expression of keratinocyte transglutaminase, hyperproliferative keratins K6 and K16, IL-6, skin-derived antileukoproteinase (SKALP), involucrin, and migration inhibitory factor-related protein (27); however, it may induce filaggrin, which is underexpressed in psoriatic skin.
Involucrin
Published in Masahiko Mori, Histochemistry of the Salivary Glands, 2019
Involucrin is a soluble protein precursor of a crosslinked enveloped protein found in stratified squamous epithelia. Its molecular weight is 92 kDa. Antigenicity of involucrin is different from that of cytokeratins. Involucrin is considered a marker for terminal differentiation of squamous cells of oral mucosa, skin,1,2 and squamous-cell tumors.3–10 Immunohistochemical studies of involucrin have been made in epithelial tumors of the oral cavity,1 urogenital organs,11 and many other types of carcinomas. Histochemical localization of involucrin in salivary gland neoplasms was different from that of keratin proteins using different monoclonal antibodies.12
The Epidermal Barrier Structure and Function of Re-Harvested Skin from Non-Scalp Donor Sites
Published in Journal of Investigative Surgery, 2023
Bohan Zhang, Peng Luo, Jiachen Sun, Dawei Li, Zhaoxing Liu, Xinzhu Liu, Hongqing Zhao, Zhisheng Li, Xiaoye Xie, Jianqiu Yang, Chuan’an Shen
The structural proteins of CE include filaggrin, loricrin, involucrin, SPRR, etc., which play a key role in providing resistance to external mechanical tension, preventing the invasion of pathogens and allergens, and preventing excessive water loss in the body.11 Filaggrin is mainly expressed in the granular layer and the transparent layer of the epidermis, which interacts with keratin intermediate filaments and aggregates to form dense keratin fiber bundles, thereby forming a flat and tough scaffold structure of keratinocytes.12 With the participation of SPRR, loricrin and involucrin cross-link with each other to form an abnormally water-insoluble CE, wrapping keratin fiber bundles and forming the unique stratum corneum barrier structure of the epidermis.12 In this study, these proteins were analyzed by IHC staining. The results revealed that the expression of CE structural proteins in the skin tended to decrease as the skin was re-harvested. As a result, the connection between keratin proteins was weakened, thus impairing the barrier function.
Baricitinib for the treatment of atopic dermatitis
Published in Journal of Dermatological Treatment, 2022
Amelia Melo, Jose Manuel Carrascosa, Tiago Torres
AD is found to present a biphasic inflammation, concerning its immune response. In the initial acute phase, a Th2-biased immune response dominates, with eosinophils, TSLP, IL-4, IL-5, IL-13, IL-31 and CCL18, associated with Th22 responses, like IL-22 and S100A proteins. These seem to downregulate terminal differentiation genes and tight junction products which causes skin barrier dysfunction (49–57). IL-4 and IL-13 are known to play a significant part in the pathogenesis of this condition and AD has been proven to be genetically related to IL-4 and IL-13 polymorphisms (58–61). In addition, in the presence of IL-4 and IL-13, keratinocytes show an appreciably decrease in filaggrin gene expression (62). IL-4 and IL-13 also downregulate loricrin and involucrin in the skin of patients with AD (53). On the other hand, there seems to be a Th1/Th0 dominance, with IL-12, IL-5, IFN-γ and GM-CSF, in the chronic phase (49,63).
Optimization of an oral mucosa in vitro model based on cell line TR146
Published in Tissue Barriers, 2020
Grace C. Lin, Tamara Leitgeb, Alexandra Vladetic, Heinz-Peter Friedl, Nadine Rhodes, Angela Rossi, Eva Roblegg, Winfried Neuhaus
In order to confirm the presence of continuous tight junctions, the localization of tight junction marker occludin was morphologically characterized using immunofluorescent staining on microscope slides (see supplementary Figure S4A). To confirm the presence of cytokeratins, differentiation markers for epithelial cells, at the protein level additionally to the mRNA level, immunofluorescent staining (K5/K8) was accomplished on microscope slides and inserts (see supplementary Figure S4A-B). In general, HE stainings showed a stratified non-keratinized epithelium, which corresponds to the phenotype of the cell line of the buccal region. Interestingly, the cornification markers (loricrin > filaggrin > involucrin) showed a high upregulation under the presence of hydrocortisone or other supplement compositions containing hydrocortisone such as HKGS and HKGS/KGF/A2P. This confirmed the enhanced differentiation upon hydrocortisone in epithelial cell layers, which was in concordance to higher TEER values of the accordingly treated TR146 inserts. In the oral epithelium, desmosomes play a pivotal role as intercellular junctions.51 Although one focus of the presented study is the comprehensive investigation of the expression of tight junction proteins, the expression of desmoglein 3, a desmosome formation facilitating protein, was evaluated with conventional qPCR (see supplementary Figure S5). Interestingly, DMEM media supplemented with 1000 nM hydrocortisone, HKGS (the optimized media) and with HKGS/KGF/A2P showed an upregulation to a similar scale compared to the biopsy samples of healthy donors.