Recent advances in epidermal cell cultures

1979 ◽  
Vol 264 (2) ◽  
pp. 243-247 ◽  
Author(s):  
Michel Prunieras
1995 ◽  
Vol 11 (4) ◽  
pp. 461-467 ◽  
Author(s):  
J. -J. Zhong ◽  
J. -T. Yu ◽  
T. Yoshida

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 612
Author(s):  
Akito Hasegawa ◽  
Riichiro Abe

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening diseases characterized by detachment of the epidermis and mucous membrane. SJS/TEN are considered to be on the same spectrum of diseases with different severities. They are classified by the percentage of skin detachment area. SJS/TEN can also cause several complications in the liver, kidneys, and respiratory tract. The pathogenesis of SJS/TEN is still unclear. Although it is difficult to diagnose early stage SJS/TEN, biomarkers for diagnosis or severity prediction have not been well established. Furthermore, optimal therapeutic options for SJS/TEN are still controversial. Several drugs, such as carbamazepine and allopurinol, are reported to have a strong relationship with a specific human leukocyte antigen (HLA) type. This relationship differs between different ethnicities. Recently, the usefulness of HLA screening before administering specific drugs to decrease the incidence of SJS/TEN has been investigated. Skin detachment in SJS/TEN skin lesions is caused by extensive epidermal cell death, which has been considered to be apoptosis via the Fas-FasL pathway or perforin/granzyme pathway. We reported that necroptosis, i.e. programmed necrosis, also contributes to epidermal cell death. Annexin A1, released from monocytes, and its interaction with the formyl peptide receptor 1 induce necroptosis. Several diagnostic or prognostic biomarkers for SJS/TEN have been reported, such as CCL-27, IL-15, galectin-7, and RIP3. Supportive care is recommended for the treatment of SJS/TEN. However, optimal therapeutic options such as systemic corticosteroids, intravenous immunoglobulin, cyclosporine, and TNF-α antagonists are still controversial. Recently, the beneficial effects of cyclosporine and TNF-α antagonists have been explored. In this review, we discuss recent advances in the pathophysiology and management of SJS/TEN.


2019 ◽  
Vol 42 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-Yi Chen ◽  
Jin-Yang Chen ◽  
Xiang-Min Tong ◽  
Jian-Guo Mei ◽  
Yun-Fang Chen ◽  
...  

1975 ◽  
Vol 93 (2) ◽  
pp. 443-457 ◽  
Author(s):  
N.E. Fusenig ◽  
P.K.M. Worst

Author(s):  
N. E. Fusenig ◽  
D. Breitkreutz ◽  
M. Lueder ◽  
P. Boukamp ◽  
P. K. M. Worst

1982 ◽  
Vol 58 (1) ◽  
pp. 49-61
Author(s):  
A.L. Kariniemi ◽  
V.P. Lehto ◽  
T. Vartio ◽  
I. Virtanen

Pure adult human keratinocyte cultures were raised from suction-blister roof epidermis and cultured in MCDB-151 medium. In primary culture the epidermal cells rapidly adhered, spread and began to proliferate on collagen-coated growth substrata but not on uncoated plastic or glass substrata. A fibrillar keratin-specific fluorescence, showing a typical cell-cell arrangement, was seen in all cells in indirect immunofluorescence microscopy, whereas only some cells also showed vimentin-specific staining. A fine fibrillar fibronectin-specific surface staining was seen at the margin of attaching cells and in marginal cells of spreading cell islands, whereas no fluorescence could be seen in epidermal cells, with antibodies against type IV collagen or laminin. Interestingly, the marginal cells also showed intracellular fibronectin. The synthesis of fibronectin in epidermal cell cultures could also be revealed by metabolic labelling experiments with [35S]methionine. In contrast to primary cultures, subcultivated keratinocytes also adhered to uncoated plastic and glass substrata. After subcultivation, keratin and surface fibronectin distribution remained unaltered but after some subcultivations, most of the cells also showed fibrillar vimentin and expressed fibronectin intracellularly. The results show that the suction-blister method provides an easy way to obtain pure epidermal cell cultures without contaminating mesenchymal cells. Our results also suggest a direct role for fibronectin but not for collagen type IV or laminin in adhesion and spreading of epidermal cells in vitro.


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