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Lung Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Daniel J. Tschumperlin, Francis Boudreault, Fei Liu
Stretch also leads to remodeling of the epithelial intermediate filament network147 and actin cytoskeleton,142 and calcium-dependent fusion of lamellar bodies with the cell membrane.148 Lamellar bodies are the densely packed structures used by cells to store and deliver the phospholipid components of pulmonary surfactant. The stretch-induced fusion of lamellar bodies builds on pioneering work that demonstrated enhanced surfactant secretion caused by stretch in vitro149 and lung inflation in situ.150 Interestingly, further studies on cell stretch in vitro demonstrate that mixed cultures of type I and type II cells respond to stretch with greater phospholipid secretion than type II cells alone, implicating type I cells as primary mechanosensors, which stimulate secretion in neighboring type II cells though extracellular ATP signaling.151
Microemulsions: Principles, Scope, Methods, and Applications in Transdermal Drug Delivery
Published in Deepak Kumar Verma, Megh R. Goyal, Hafiz Ansar Rasul Suleria, Nanotechnology and Nanomaterial Applications in Food, Health, and Biomedical Sciences, 2019
Irina Pereira, Sara Antunes, Ana C. Santos, Francisco J. Veiga, Amélia M. Silva, Prapaporn Boonme, Eliana B. Souto
Stratum corneum (SC) is the epidermis outermost strata and contributes primarily to the barrier function of the skin. This stratum is characterized by a thin layer of squamous cells organized in a dense configuration with specialized lipids in the intercellular spaces, and with an acid pH character. The SC is constituted by layers of flattened cells designated by corneocytes. The life cycle of these cells starts as keratinocytes in the basal layer of epidermis, followed by their displacement along time through the numerous layers of epidermis until reaching the skin surface. Once at this stage, they have been differentiated to nonliving pancake-flat cells called corneocytes, which are tightly bound into sheets. When they reach the outermost layer of the SC, corneocytes shed and their life cycle starts over again. The dense and thick layer with 15–20 μm of corneocytes in the skin is responsible for providing the physical barrier protection.66,88 Under the SC, there is an impermeable lipid-based layer that is tightly stacked to corneocytes. These lipids, originating from unique epidermis structures called lamellar bodies, are structured in bilayers and consist of ceramides; cholesterol, and essential fatty acids. This lipid mixture layer plays a key role on the proper skin barrier function by the prevention of water loss, and also by avoiding the entrance of undesirable substances.28,81 Where the lipid layer integrity is affected, the skin barrier function is disrupted causing dehydration. This compromises the normal shedding of cells from the SC surface, and, consequently, the skin becomes dry and flaky.
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
The FLG monomers take part in SC formation. In this process, FLG monomers bind to keratin filaments, aggregating them into keratin fibrils organized in parallel bundles to form a matrix that provides rigidity to the overall structure, which are the major constituents of corneocytes (Egawa and Kabashima 2018; Norlén and Al-Amoudi 2004). Corneocytes generate a network within a lipid-rich extracellular matrix and produce compaction of keratinocytes. In the process of compacting keratinocytes, corneocytes are denucleated and flattened, and the intercellular space between them filled with lipids from the lamellar bodies (Egawa and Kabashima 2018). Lamellar bodies are membrane-circumscribed granules produced by keratinocytes from SG and contain lipids, corneodesmosin, and kallikreins (Egawa and Kabashima 2018). These lipids are mainly ceramides, free fatty acids, and cholesterol. The secretion of the content of lamellar bodies into the extracellular space enables the covalent attachment of o-hydroxylated ceramides and fatty acids to cornified envelope proteins, forming a lipid-bound envelope (Hill, Paslin, and Wertz 2006). Then, lysosomal enzymes, which need an acidic pH optimum, degrade the polar lipid precursor to hydrophobic ceramides, generating an intact permeability barrier, and is responsible for the acidic pH of the skin (Doering et al. 1999).