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Epidermal keratinocytes

Hanson, D. and De Leo, V.A. (1990). Long-wave ultraviolet light induces phospholipase activation in cultured human epidermal keratinocytes. J. Invest. Dermatol. 95, 158-163. [Pg.122]

MWNTs were found to be cytotoxic in human skin fibroblasts (HSF42) and human epidermal keratinocytes (HEK) [42-44], whereas SWNTs were toxic in human keratinocyte (HaCaT) cultures [25, 26, 45]. Reduced cell proliferation and oxidative stress were reported also in epithelial (HeLa) cells [45] and murine epidermal cells (JB6 P + ) [46] upon incubation with SWNTs. [Pg.181]

Zhang, L.W. et al. (2007) Biological interactions of functionalized single-wall carbon nanotubes in human epidermal keratinocytes. International Journal of Toxicology, 26 (2), 103-113. [Pg.210]

Monteiro-Riviere, N.A. et al. (2005) Multi-walled carbon nanotube interactions with human epidermal keratinocytes. Toxicology Letters, 155 (3), 377—384. [Pg.210]

Zollanvari, A. et al. (2009) Analysis and modeling of time-course gene-expression profiles from nanomaterial-exposed primary human epidermal keratinocytes. BMC Bioinformatics, 10, (Suppl. 11) S10. [Pg.211]

Based on observations in JP-8 inhalation studies, the protective role of SP in dermal toxicity was recently examined. As mentioned earlier, inhalation exposure to JP-8 and SP resulted in protection from of lung toxicity and restoration of immune function [24,25,26], Similarily, co-administration of substance P (SP) with JP-8 also decreased toxicity in human epidermal keratinocytes[27]. This suggests that a common... [Pg.229]

Shopsis, C. (1989). Validation study ocular irritancy prediction with the total cell protein, uridine uptake, and neutral red assays applied to human epidermal keratinocytes and mouse 3t3 cells. In Alternative Methods in Toxicology, Vol. 7 (Goldberg, A.M., Ed.). Mary Arm Liebert, New York, pp. 273-287. [Pg.687]

Recently, the possibility to use C60 as anti-inflammatory compound has been reported (Huang et al., 2008). Fullerene-xanthine hybrids have been studied to determine if nitric oxide (NO) and tumor necrosis factor-alpha (TNF-a) production in lipopolysaccharide (LPS)-activated macrophages can be inhibited by hybrid administration, finding positive results. The presence of xanthine moiety seems to be essential for the inhibition of LPS-induced TNF-a production, while the fullerene portion ameliorates the efficiency in LPS-induced NO production blockage, leading to a new promising class of potent anti-inflammatoiy agents. It is necessary to mention also the opposite results obtained by an amino acid fullerene derivative tested on human epidermal keratinocytes at concentration from 0.4 to 400 pg/mL. [Pg.6]

Rouse JG, Yang J, Barron AR, Monteiro-Riviere NA (2006) Fullerene-based amino acid nanoparticle interactions with human epidermal keratinocytes. Toxicol. In Vitro 20 1313-1320. [Pg.20]

Wilmer JL, Burleson FG, Kayama F, et al. 1994. Cytokine induction in human epidermal keratinocytes exposed to contact irritants and its relation to chemical-induced inflammation in mouse skin. J Invest Dermatol 102 915-922. [Pg.231]

Shvedova, A.A., Tyurina, Y.Y., Kawai, K., Tyurin, V.A., Kommineni, C., Fabisiak, J.P., and Kagan, V.E., 2001, Selective peroxidation and extemalization of phosphatidylserine in normal human epidermal keratinocytes during oxidative stress induced by cumene hydroperoxide, J. Inv. Derm, (submitted for publication). [Pg.95]

The EpiDerm (EPI-200) skin model is mechanistically and functionally related to EPISKIN. The assay consists of normal human epidermal keratinocytes, which have been cultured in a chemically defined medium to produce a stratified, highly diEerentiated, organotypic tissue model of the human epidermis. [Pg.60]

Studies carried out with complete cells in vivo, cell membranes and other cell fractions point to the selective oxidation of phosphatidylserine (26) to a hydroperoxide (PS-OOH) on oxidative stress caused by toxic agents such as H2O2, t-BuOOH and cumyl hydroperoxide (27). Formation of PS-OOH is observed during apoptosis. These phenomena are important because of the cytotoxic effects of various peroxides used in commercial products coming into direct contact with the human body, as is the case of epidermal keratinocytes in contact with cosmetic formulations" ". The toxic effects of f-BuOOH are associated with vasoconstriction and damage to the vascular smooth muscles ". Global determination methods for primary lipid oxidation products are discussed in Section IV.B. [Pg.613]

Calcipotriol is a vitamin D3 derivative which is used as a topical agent in the treatment of psoriasis. Although not completely elucidated its mechanism of action seems to be based on inhibition of the proliferation and stimulation of the differentiation of epidermal keratinocytes. Adverse effects include irritation of the skin but also urticarial reactions. Calcipotriol has 100 fold less vitamin D activity as its active vitamin D3 metabolite calcitriol. However, calcipotriol in overdose can cause symptoms of hypercalcemia. [Pg.482]

Monteiro-Riviere NA, Nemanich RJ, Inman AO et al (2005) Multi-walled carbon nanotube interactionwith human epidermal keratinocytes. Toxicol Lett 155 377-384... [Pg.21]

Rheinwald JG, Green H (1975) Serial cultivation of strains of human epidermal keratinocytes the formation of keratinizing colonies from single cells. Cell 6(3) 331-343... [Pg.255]

A novel IFN (IFN-k) with 30% homology to other type I proteins has been identified in epidermal keratinocytes. IFN-k gene is located on chromosome 9, and its protein consists of 207 amino acids. It is induced in keratinocytes upon viral infection, exposure to double stranded RNA, IFN-y, or IFN-(i. It imparts cellular protec-... [Pg.167]

Methyl methanesulfonate induced DNA single-strand breaks and alkali-labile sites in human lymphocytes in vitro. It induced unscheduled DNA synthesis in human epidermal keratinocytes and in oral epithelial and fibroblast cell cultures. Methyl methanesulfonate induced gene mutations in human lymphoblasts at the hprt locus and sister chromatid exchanges and micronuclei in HepG2 human liver cells in vitro. [Pg.1063]

Katiyar SK, Afaq F, Azizuddin K, Mukhtar H. 2001. Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (—)-epigallocatechin-3-gallate. Toxicol Appl Pharmacol 176 110-117. [Pg.180]

Brown LF, Yeo KT, Berse B, Yeo TK, Senger DR, Dvorak HF, Van de Water L. 1992. Expression of vascular permeability factor (vascular endothelial growth factor) by epidermal keratinocytes during wound healing. J Exp Med 176 1375-1379. [Pg.321]

Vega, L Styblo, M., Patterson, R. et al. (2001) Differential effects of trivalent and pentavalent arsenicals on cell proliferation and cytokine secretion in normal human epidermal keratinocytes. Toxicology and Applied Pharmacology, 172(3), 225-32. [Pg.273]

Steven, A.C., et al. 1990. Biosynthetic pathways of filaggrin and loricrin—two major proteins expressed by terminally differentiated epidermal keratinocytes. J Struct Biol 104 150. [Pg.228]

It has been recently demonstrated (Sakaguchi et al., 2004 Sakaguchi et al., 2003 Sakaguchi et al., 2005) that S100A11 is a key mediator for growth inhibition of normal human epidermal keratinocytes (NHK) triggered by high Ca2+ or TGF(3. [Pg.113]

Sakaguchi M, Miyazaki M, Takaishi M, Sakaguchi Y, Makino E, Rataoka N, Yamada H, Namba M, Huh NH. 2003. S100C/A11 is a key mediator of Ca(2+)-induced growth inhibition of human epidermal keratinocytes. J Cell Biol 163(4) 825—835. [Pg.134]

Ny A, Egelrud T. Transgenic mice over-expressing a serine protease in the skin Evidence of interferon gamma-independent MHC II expression by epidermal keratinocytes. Acta Derm Venereol 2003 83 322-327. [Pg.76]

The stratum corneum consists of denucleated corneocytes filled with cross-linked proteins, while the intercellular space is occupied by lipids synthesized prior to and during cornification [24], Formation of this barrier relies on the cornification of epidermal keratinocytes, which undergo growth arrest, terminal differentiation, and an epidermal-specific cell death, referred to as planned cell death [25], Abnormalities in any of these programmed events may lead to epidermal disorders such as psoriasis, atopic dermatitis, and cancer. Flowever, biological events that enable basal cells (stem cells) to proliferate, differentiate, and commit planned cell death are still poorly understood [10]. The keratinocyte differentiation process can be stimulated by prodifferentiation agents such as extracellular calcium and 1,25-dihydroxy cholecalciferol (referred to as vitamin D3 hereafter) [23], Aberrant or absent differentiation can be found in other skin disorders such as atopic keratosis, seborrheic keratosis, and rosacea. [Pg.124]


See other pages where Epidermal keratinocytes is mentioned: [Pg.428]    [Pg.1429]    [Pg.236]    [Pg.283]    [Pg.114]    [Pg.293]    [Pg.124]    [Pg.613]    [Pg.296]    [Pg.1063]    [Pg.174]    [Pg.340]    [Pg.23]    [Pg.319]    [Pg.102]    [Pg.108]    [Pg.390]    [Pg.400]    [Pg.337]    [Pg.120]    [Pg.120]    [Pg.123]   
See also in sourсe #XX -- [ Pg.56 ]




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Epidermal

Human epidermal keratinocytes

Keratinocyte

Keratinocytes

Normal human epidermal keratinocytes

Normal human epidermal keratinocytes NHEKs)

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