Extracellular matrix and keratinocyte migration
We are just beginning to understand some of the cellular mechanisms involved in human keratinocyte migration on extracellular matrix. Extracellular matrix components have differing effects on keratinocyte motility. Signalling through integrin receptors and secretion of collagenase are both components of this process. An understanding of the effect of extracellular matrix on keratinocyte migration has direct relevance to the problem of wound re‐epithelialization and will assist in the development of therapeutic efforts to enhance wound healing artificially. [1]
Mutations of keratinocyte transglutaminase in lamellar ichthyosis
Lamellar ichthyosis is a severe congenital skin disorder characterized by generalized large scales and variable redness. Affected individuals in three families exhibited drastically reduced keratinocyte transglutaminase (TGK) activity. In two of these families, expression of TGK transcripts was diminished or abnormal and no TGK protein was detected. Homozygous or compound heterozygous mutations of the TGK gene were identified in all families. These data suggest that defects in TGK cause lamellar ichthyosis and that intact cross-linkage of cornified cell envelopes is required for epidermal tissue homeostasis. [2]
Cytokine Modulation of Keratinocyte Cytokines
There is increasing evidence that epidermal cytokines may have an important role in mediating inflammatory and immune responses in the skin. A number of cell types in the epidermis are capable of secreting cytokines including keratinocytes, Langerhans cells, melanocytic cells, and even Merkle cells. Keratinocytes are the major source of cytokines in the epidermis and have been reported to secrete IL-1, IL-3, IL-6, IL-8, CSF, TNFα, TGFα, TGFβ, and PDGF. Normally these cytokines are not actively secreted by keratinocytes; however, a number of agents are capable of mediating keratinocyte cytokine production, including cytokines themselves. We examined the effect of a number of cytokines on keratinocyte IL-1, IL-6, GM-CSF, and PDGF production. [3]
Assessment of the Role of NO Synthase Genes Polymorphisms in the Pathogenesis of Psoriasis
Aims: Psoriasis is a common (affecting 2% of the general population) chronic inflammatory skin disease characterized by impaired keratinocyte differentiation and proliferation. Nitric oxide (NO) is one of the most potent vasodilators synthesized in large quantities at the early stages of wound response, as well as in inflammation. Psoriasis has been shown to be associated with increased NO content in pathological tissues. The objective of this study was to analyze two single-nucleotide substitutions in the NOS2 (rs2779249, c.-1290G>T, 5’-region) and NOS3 (rs2070744, c.-813C>T, intron 1) genes. [4]
Reference
[1] O’toole, E.A., 2001. Extracellular matrix and keratinocyte migration. Clinical and experimental dermatology, 26(6), pp.525-530.
[2] Huber, M., Rettler, I., Bernasconi, K., Frenk, E., Lavrijsen, S.P., Ponec, M., Bon, A., Lautenschlager, S., Schorderet, D.F. and Hohl, D., 1995. Mutations of keratinocyte transglutaminase in lamellar ichthyosis. Science, 267(5197), pp.525-528.
[3] Ansel, J., Perry, P., Brown, J., Damm, D., Phan, T., Hart, C., Luger, T. and Hefeneider, S., 1990. Cytokine modulation of keratinocyte cytokines. Journal of Investigative Dermatology, 94(6), pp.s101-s107.
[4] Klimov, E., Tretiakov, A., Gapanovich, E., Kokaeva, Z., Soboleva, A., Sakaniya, L., Korsunskaya, I. and Sobolev, V., 2018. Assessment of the Role of NO Synthase Genes Polymorphisms in the Pathogenesis of Psoriasis. Journal of Advances in Medicine and Medical Research, pp.1-6.