Development of the sulfur mustard resistant keratinocyte cell line HaCaT/SM
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HaCaT
Sulfur mustard
目的将为决定 P63 是否是 proliferative 潜力 keratinocytes 的标记在特别 keratinocyte 原版 hyperproliferate 疾病和变化房间类型的纸巾检验 p63 的表示模式。方法 P63 蛋白质被检测并且包括有鳞的房间癌 SCC ，基础房间癌电子消息传输方式，鲍恩的疾病和另外的纸巾或房间在 keratinocyte 原版混乱的活体检视标本由 immunoreactivity 方法和西方的污点分析了，例如干癣 vulgaris ，正常的皮纸巾，主要有教养的 keratinocytes ，不朽的 HaCaT 房间，和表皮状的癌房间 A431 。结果 P63 蛋白质在原子核被表示基础并且外皮的 suprabasal 层，在正常的油脂的腺的发芽房间表皮。P63 强烈并且广泛地在电子消息传输方式和糟糕区分的 SCC 在肿瘤房间的多数被检测。在鲍恩的疾病， p63 快车在所有房间层是显著的。在干癣匾表皮，主要在难弄的房间的基础房间和部分表示的 p63。P63 比在 A431 房间或 HaCaT 房间在主要有教养的 keratinocytes 强烈表示了更多。结论 P63 是有 proliferative 潜力的无差别的 keratinocytes 的一个原子核标记并且可以破坏终端区别。p63 的 overexpression 反映肿瘤房间的未成熟。p63 染色的 immunohistochemical 可能为调查肿瘤房间的起源和区别是有用的。
HaCaT
A431 cells
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Earthworm, Eutyphoeus gammiei, homogenate (EGH) was screened for wound healing activity on human keratinocyte cell line, HaCat, by cell proliferation and migration assays. The maximum proliferation and migration of keratinocyte cells were observed at the dose of 25μg/ml. As cell proliferation and migration are key factors for wound healing, the study clearly suggests the potential role of earthworm species Eutyphoeus gammiei on wound healing.
Keywords: Eutyphoeus gammiei, Keratinocyte, MTT assay, scratch assay.
HaCaT
MTT assay
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The insulin-like growth factor receptor (IGF-IR) is critical in epidermal development and IGF binding protein-3 (IGFBP-3), a modulator of cellular activity with or without IGF-dependence, co-localises with epidermal IGF-IRs. We have investigated whether the greater UV susceptibility of a human keratinocyte cell line (HaCaT) in comparison to normal human keratinocytes (NHKs) may involve differences in the IGF system. At 24 h after UV (960 mJ/cm2 UVB), in comparison to NHKs, HaCaT keratinocytes exhibited significantly higher levels of apoptosis, refractoriness to IGF-I treatment and reduced IGF-IR phosphorylation. Secreted, intact IGFBP-3 (38–42 kDa) and IGFBP-3 mRNA abundance were reduced in HaCaT keratinocytes, but not consistently altered in NHKs. Immunoreactive IGFBP-3 fragments (16–11 kDa) were detected in both UV-exposed cultures. These data suggest that an altered IGF system contributes to HaCaT keratinocyte UV susceptibility and that following UV insult the IGF system may enhance keratinocyte viability and contribute to a return to epidermal homeostasis.
HaCaT
Human skin
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Proliferation and migration of keratinocytes are vital processes for the successful epithelization specifically after wounding. MiR-221 has been identified to play a potential role in promoting wound regeneration by inducing blood vessel formation. However, little is known about the role of miR-221 in the keratinocyte proliferation and migration during wound healing. An in vivo mice wound-healing model was generated; the expression levels of miR-221 were assessed by qRT-PCR and fluorescence in situ hybridization. Initially, we found that miR-221 was upregulated in the proliferative phase of wound healing. Further, in an in vivo wound-healing mice model, targeted delivery of miR-221 mimics accelerated wound healing. Contrastingly, inhibition of miR-221 delayed healing. Additionally, we observed that overexpression of miR-221 promoted cell proliferation and migration, while inhibition of miR-221 had the opposite effects. Moreover, we identified SOCS7 as a direct target of miR-221 in keratinocytes and overexpression of SOCS7 reversed the effects of miR-221 in HaCaT keratinocytes. Finally, we identified that YB-1 regulates the expression of miR-221 in HaCaT keratinocytes. Overall, our experiments suggest that miR-221 is regulated by YB-1 in HaCaT keratinocytes and acts on SOCS7, thereby playing an important role in HaCaT keratinocyte proliferation and migration during wound healing.
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Reaction of elemental sulfur in ethylenediamine with 1,1-thiobis(2-chloroethane) or sulfur mustard, the potent chemical warfare agent has been studied. The optimum conditions for the reaction are established for the complete conversion of sulfur mustard into non-toxic products. The above reaction has been successfully converted into a technology for chemical destruction of sulfur mustard (patented in USA, Russia, Germany and India).
Sulfur mustard
Ethylene diamine
Nitrogen mustard
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HaCaT
Immortalised cell line
Epidermis (zoology)
Human skin
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The primary function of the skin is to protect the body from the unwanted environmental influences. The outermost layer of the skin is stratum corneum which consists of corneocytes surrounded by lipid regions. Ceramides covalently bound to keratinocytes are essential for the barrier function of the skin, which can be disturbed in the disease, like xerosis. Xerosis is an abnormal dryness of the skin which reduced the thickness of stratum corneum and ceramide content decreasing with age. In this study, 36 seaweed extracts have been tested for screening of xerosis inhibitory agent by in vitro HaCaT keratinocyte assay. Ishige sinicola and Helminthocladia australis induced the significant amount of ceramide-like substance I in HaCaT keratinocyte among the tested seaweed extracts. Sargassum fulvellum, Chondrus ecellatus and Gigartina tenella also induced the ceramide-like substance I whereas Helminthocladia australis and Pachymeniopsis elliptica induced the ceramide-like II from HaCaT keratinocyte.
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Corneocyte
Barrier function
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We have studied the gap junctional intercellular communication (GJIC) of immortalized and tumourigenic human keratinocyte cell lines and of a spontaneously immortalized non-tumourigenic and a highly differentiating keratinocyte cell line (HaCaT) as the control. In homologous cultures, the GJIC capacity of five squamous cell carcinoma-derived cell lines was 1-27% that of the HaCaT cells. Ha-ras-transfected HaCaT cells with tumourigenic potential and an SV40 DNA-immortalized cell line had markedly reduced GJIC capacities. Northern analysis and immunohistochemistry showed that connexin (Cx) 43 is the major gap junction protein expressed in the communicating cells. They do not express Cx 26 or 32. The low or absent communication observed in certain cell lines was due in some to a lack of Cx 43 gene expression, but in others to aberrant localization of the gap junction protein. GJIC of these cell lines, as well as that of primary normal human epidermal keratinocytes, was susceptible to 12-O-tetradecanoylphorbol-13-acetate-mediated inhibition. Moreover, GJIC of HaCaT cells and their tumourigenic derivatives is Ca(2+)-dependent. These results, when compared with those previously obtained for mouse keratinocyte cell lines, reveal that GJIC of human keratinocytes was correlated to the degree of differentiation and is controlled in a similar way to that of murine keratinocytes. Aberrant GJIC seems to be a common feature of human and murine skin carcinogenesis.
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Immortalised cell line
Cell type
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Effect of Yinxieling Prescription and Its Modified Prescriptions on Keratinocyte HaCaT Proliferation
Objective To observe the effect of Yinxieling Prescription(YP)and its modified prescriptions on keratinocyte HaCaT proliferation,and to screen the effective components of YP.Methods Orthogonal design was adopted for the preparation of 12 modified prescriptions of YP.With lipopolysaccharide(LPS) as the stimulating factor,human in-vitro hyperproliferation keratinocyte HaCaT model was established.The effect of YP and its modified prescriptions at different concentrations on the proliferation of keratinocyte HaCaT was examined by methyl thiazolyl tetrazolium(MTT)assay.The correlation of effect with time was also investigated.Results YP had inhibitory effect on the proliferation of keratinocyte HaCaT,and the effect was correlated with the concentration and action time.Modified prescriptions 7 and 8 inhibited the proliferation of keratinocyte HaCaT obviously,and the difference was significant as compared with LPS model group(P0.05).Conclusion The therapeutic mechanism of YP for psoriasis may be related with the inhibition of keratinocyte HaCaT proliferation,and the components of modified prescriptions 7 and 8 probably are the effective components of YP.
HaCaT
MTT assay
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