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Skin
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
The spinous cell layer overlies the basal cell layer and is the thickest layer of the epidermis. It is composed of polyhedral to flattened cells containing large numbers of desmosomes that interdigitate with each other via intercellular bridges, giving this layer a “prickle cell” or “spinous” appearance. Similar to basal cells, cells of the spinous cell layer contain free ribosomes, RER, and a Golgi apparatus, but in contrast to basal cells, they contain more tonofilaments (i.e., cytokeratin) that radiate outward from the perinuclear area to the interdigitated cellular processes that bridge the intercellular spaces. As keratinocytes of the spinous cell layer move outward, they continue to produce tonofilaments that collect together to form tonofibrils contributing to the eosinophilic appearance of these cells. These keratinocytes also contain cytoplasmic membrane-coated granules (also known as lamellar granules), which are flattened vesicles containing complex lipids, proteases, and lipases (the latter of which are involved in desquamation) and are typically arranged in a lamellar pattern (Fartasch 2004). In general, keratinocytes in the basal levels of the spinous cell layer are mitotically active only when the skin is responding to injury; thus, suprabasilar mitoses are indicative of ongoing epidermal proliferation and are characteristic of certain chronic skin conditions.
Integrin Receptors and Epiligrin in Cell-Cell and Cell-Substrate Adhesion in the Epidermis
Published in Yoshikazu Takada, Integrins: The Biological Problems, 2017
William G. Carter, Susana G. Gil, Banu E. Symington, Tod A. Brown, Shunji Hattori, Maureen C. Ryan
Desmosomes are relatively few in the basal cell layer but are upregulated in the suprabasal and spinous cell layer. Consistently, serum from patients with the autoimmune blistering disorder Pemphigus vulgaris (PV) express autoantibodies that cause detachment of suprabasal cells from the basal cells. Recently, the PV antigen was shown to be identical to desmoglein, a desmosomal Cadherin (Amagai et al., 1991). The PV antigen, like the desmosomes, is upregulated in the suprabasal cell layer where it is a target for the autoimmune antibodies (Karpati et al., 1993).
Increased expression of TGF-β protein in the lesional skins of melasma patients following treatment with platelet-rich plasma
Published in Journal of Cosmetic and Laser Therapy, 2019
Eman R. M. Hofny, Mahmoud Rezk Abdelwahed Hussein, Alaa Ghazally, Asmaa M. Ahmed, Amira A. Abdel-Motaleb
In the appendicular tissue specimens (positive control), TGF-β protein expression was seen as a strong cytoplasmic staining in the lining mucosal epithelial cells and in the lymphocytes of the lamina propria. The expression was also observed in the fibroblasts and endothelial cells lining the walls of the blood vessels. Weak expression was noticed in the muscle fibers and nerve plexuses. A summary of these findings is shown in Figure 1. In the healthy skins (control group), TGF-β protein expression was observed throughout the epidermis, in the dermal adnexal structures, vascular endothelium, nerves and in the arrector pili muscle fibers. In the epidermis, the expression values were higher in the basal cell keratinocytes (2.33 ± 0.71) than in the other epidermal layers (spinous cell, granular cell, and horny cell layers: 2.11 ± 0.60). The mean value of TGF-β protein expression in the epidermis was 2.17 ± 0.60. As compared to the healthy skin, the expression values of TGF-β protein were lower in the perilesional skin. In the epidermis, the values ranged from 1.60 ± 0.70 (prickle cells keratinocytes) to 1.70 ± 0.68 (basal cell keratinocytes). Similarly, the expression in the dermal adnexa, fibroblasts, endothelial cells and lymphocytes were low as compared to the healthy skin. A summary of these findings is presented in Tables 2 and 3 and in Figures 2 and 3.