Inhibitory action of cholesterol addition to tween 60 on the tumor promoting and epidermal hyperplasia causing effects in mouse skin

1959 ◽  
Vol 46 (9) ◽  
pp. 331-331 ◽  
Author(s):  
Kai Set�l� ◽  
Lauri Merenmies ◽  
Yrj� Aho ◽  
Leo Stjernvall ◽  
Onerva �yr�p��
2006 ◽  
Vol 203 (12) ◽  
pp. 2577-2587 ◽  
Author(s):  
Jason R. Chan ◽  
Wendy Blumenschein ◽  
Erin Murphy ◽  
Caroline Diveu ◽  
Maria Wiekowski ◽  
...  

Aberrant cytokine expression has been proposed as an underlying cause of psoriasis, although it is unclear which cytokines play critical roles. Interleukin (IL)-23 is expressed in human psoriasis and may be a master regulator cytokine. Direct intradermal administration of IL-23 in mouse skin, but not IL-12, initiates a tumor necrosis factor–dependent, but IL-17A–independent, cascade of events resulting in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis. IL-23 induced IL-19 and IL-24 expression in mouse skin, and both genes were also elevated in human psoriasis. IL-23–dependent epidermal hyperplasia was observed in IL-19−/− and IL-24−/− mice, but was inhibited in IL-20R2−/− mice. These data implicate IL-23 in the pathogenesis of psoriasis and support IL-20R2 as a novel therapeutic target.


1989 ◽  
Vol 8 (2) ◽  
pp. 245-251
Author(s):  
Jeffrey D. Laskin

Keratins are the major proteins synthesized by keratinocytes. They consist of a group of 10–20 different polypeptides in the molecular weight range of 48,000–67,000. Keratins associate in cells to form intermediate filaments, the major network of the keratinocyte cytoskeletal architecture. Keratins are produced in cells in a specific, sequential manner during epidermal stratification and the formation of the stratum corneum. Tumor promotion in mouse skin is associated with epidermal hyperplasia and aberrant cellular differentiation. This is accompanied by alterations in normal patterns of keratinization as revealed by high-resolution two-dimensional polyacrylamide gel electrophoresis. Changes in keratinization in mouse skin during tumor promotion may serve as useful markers for the development of neoplasia.


1986 ◽  
Vol 72 (6) ◽  
pp. 643-650 ◽  
Author(s):  
Rajani A. Bhisey ◽  
Satyavati M. Sirsat

Stationary epidermal hyperplasia induced by exposure of mouse skin to 1-6 TPA applications was analyzed by electron microscopy and found to be of two types. Intermingled orderly and irregularly stratified hyperplastic regions observed prominently after a single TPA application gave way, on multiple treatment, to epidermal hyperplasia populated by either cuboidal cells with expanded cytoplasm or by highly polar, narrow, tall and pleomorphic cells. Both cell types were poorly differentiated and displayed a paucity of intact desmosomal junctions, resulting in an incohesive tissue structure in which a number of phenotypic variants were expressed. The variants were markedly less mature than the adjacent cells and showed basal cell phenotype, acquisition of secretory activity or a disturbed mitotic process, resulting in the formation of binucleated cells. The observations suggest that the disturbed mitotic process, poor cellular differentiation and induction of metaplasia could be the mode by which an initiated cell may express its tumor phenotype and escape differentiation during the early stage of TPA promotion.


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