ABSTRACT
Objective To investigate the mechanisms of tacrolimus on the migration of Langerhans′ cells. Methods The concentration of MCP-1 in the cultured supernatants of HaCaT cell treated with tacrolimus was determined by ELISA. The expression level of MCP-1 mRNA in HaCaT cell treated with tacrolimus was studied by RT-PCR method. Results The concentration of MCP-1 in HaCaT cell treated with 625 ～ 5 000 ng/mL of tacrolimus was significantly decreased. The expression level of MCP-1 mRNA was also markedly decreased. Conclusions Tacrolimus may probably decrease the expression of MCP-1 in keratinocytes and suppress the chemotactic ability of Langerhans′ cells precursor and Langerhans′ cells, thus inhibiting or diminishing certain local immunoreaction.
ABSTRACT
Objective To investigate the regulatory effect of calcitonin gene-related peptide (CGRP) on the mRNA and protein expression of neuronal nitric oxide synthase (NOS), as well as the release of nitric oxide (NO) in cultured human keratinocyte line HaCaT. Methods NO level in the supernatant of cell culture medium was detected with an enzymatic NO detecting kit, the mRNA expression of neuronal NOS was studied with reverse transcription polymerase chain reaction(RT-PCR), and the protein expression of neuronal NOS was studied with immunochemical technique(SP). Results Compared with that in normal culture condition, the mRNA and protein expression of neuronal NOS and the release of NO was significantly upregulated by CGRP in HaCaT cells. Whereas, the expression of neuronal NOS and the release of NO in HaCaT cells induced by CGRP was inhibited by CGRP-8-37, an inhibitor of CGRP receptor. Conclusion The expression of neuronal NOS in keratinocytes and the release of NO from keratinocytes could be upregulated by CGRP.
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Objective To study the mRNA expression and function of TGF-?1, TGF-?RⅡ and CD105 in the lesional, non-lesional skin of psoriasis and of normal human skin. Methods The RNA of skin tissue was extracted using single-step method of RNA isolation by acid guanidinium thiocyanate. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure the expression of mRNA. Results The mRNA expression of TGF-?1 and TGF-?RⅡ was lower in the epidermis of psoriatic lesion than that of non-lesional psoriatic and normal human skin(P
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Objective To investigate the expression and im plication of cell-cycle related factors(Cyclin D1,CDK4,P16 MTS1 and PRb)in condyloma acuminatum(CA).Methods The expression and distribution of cyclin D1,CDK4,P16 MTS1 and PRb were detected by immunohisto chemical technique streptavidin peroxidase(SP)in 27cases of HPV6/11positive CA that were confirmed by PCR and 10cases of norm al skins(foreskins).Results①Cyclin D1was not expressed in both normal skin and lesions of CA.②The intensity of expression of CDK4was 2.19in the basal cells in the lesions of CA,which was significantly weaker than that in normal skin(4.8,P
ABSTRACT
Objective To investigate the expression of IL-8 and CXCR2 on keratinocytes from psoriatic lesions and their roles on clinical and pathologic manifestations. Methods The chemotaxis of psoriatic lesional keratinocytes was detected by micropore loculus test. The concentration of IL-8 was determined in the cultured supernatants of psoriatic keratinocytes by ELISA. The expression of CXCR2 on keratinocytes from affected skin was tested by flow cytometry. Results The chemotaxis for neutrophils by the cultured supernatants of psoriatic lesional keratinocytes was significantly stronger than that by controls. The concentration of IL-8 in the cultured supernatants of psoriatic lesional keratinocytes was also increased. The expression of CXCR2 on psoriatic keratinocytes was significantly increased. Conclusions The psoriatic epidermal hyperproliferation may be correlated with up regulation of IL-8 production and CXCR2 expression on psoriatic keratinocytes. At the same time, the psoriatic inflammation may be partly related to the increase of secretion of IL-8, which has chemotactic capacity, by keratinocytes. IL-8 and CXCR2 may be involved in the pathogenesis of psoriasis.