Epidermal Barriers

Abstract

The epidermis functions as a physical barrier to the external environment and works to prevent loss of water from the skin. Numerous factors have been implicated in the formation of epidermal barriers, such as cornified envelopes, corneocytes, lipids, junctional proteins, proteases, protease inhibitors, antimicrobial peptides, and transcription factors. This review illustrates human diseases (ichthyoses) and animal models in which the epidermal barrier is disrupted or dysfunctional at steady state owing to ablation of one or more of the above factors. These diseases and animal models help us to understand the complicated mechanisms of epidermal barrier formation and give further insights on epidermal development.

Skin microbiota–host interactions

“…In the skin, epithelial homeostasis is a constant, active, and energy-intensive process that involves the secretion of complex lipids for signalling and barrier purposes 2,66 , maintenance of tight junctions 67,68 and production of a lipid–protein coat to prevent trans-epidermal water loss 69,70 , repair of UV-mediated and oxidative damage to epithelial cells to prevent malignant transformation 71,72 , and constant remediation of accidental trauma (for example, scrapes, cuts, and nicks). Any disruption of even a small component of these complex processes can result in extreme phenotypes, such as ichthyoses, blistering disorders, progerias, and diffuse fibrosis 69,73,74 .…”

Altered epidermal lipid processing and calcium distribution in the KID syndrome mouse model Cx26S17F

“…The main function of the multilayered epidermis is to maintain a barrier which prevents water, bacteria and toxin penetration as well as water loss from the body. This epidermal barrier is mainly established by the cornified envelope and the extracellular lipid lamellae of the stratum corneum [2]. Besides free fatty acids, cholesterol and cholesterol esters, the main component of the extracellular lipid lamellae of the stratum corneum are ceramides, which show a large diversity in their acyl residues as well as in the degree of saturation of their long chain base residues [3,4].…”

Epidermal aspects of type VII collagen: Implications for dystrophic epidermolysis bullosa and epidermolysis bullosa acquisita

“…Epidermal keratinocytes maintain proliferative potential at the epidermal basal layer and are a source of stem cells that render commitment to differentiation in the suprabasal layer, which fosters epidermal barrier formation . ECM and basement membrane zone proteins including α6 integrin, β1 integrin and COL17 create a niche for epidermal stem cell maintenance through mechanical support and/or stabilization of signaling molecules .…”

“…Epidermal keratinocytes maintain proliferative potential at the epidermal basal layer and are a source of stem cells that render commitment to differentiation in the suprabasal layer, which fosters epidermal barrier formation. 52,53 ECM and basement membrane zone proteins including a6 integrin, b1 integrin and COL17 create a niche for epidermal stem cell maintenance through mechanical support and/or stabilization of signaling molecules. 51,[54][55][56] The role of COL7 in maintaining keratinocyte homeostasis has been explored in this context, mainly using in vitro cultured cells; however, keratinocytes may not be in direct contact with COL7 in situ in steady state conditions.…”