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ABSTRACT: This study examined the roles of HLA-G in the pathogenesis, development and immune tolerance of hemangioma. From 2000 to 2007, 52 paraffin-embedded specimens (26 from males and 26 from females) of skin capillary hemangioma and 7 samples of adjacent normal skin tissues were collected. Four fresh specimens of hemangioma were also harvested. All samples were HE-stained and proliferative cell nuclear antigen (PCNA) was immunohistochemically detected by using SP method. The samples were classified into proliferative group and degenerative group according to the Mulliken criteria and the expression pattern of PCNA. SP method and quantum dots double staining were applied to detect the expression of HLA-G and PCNA in hemangioma and normal tissue samples. The expression of HLA-G was detected by RT-PCR. The results showed that among the 52 samples of hemangioma, 29 were of proliferative type and 23 degenerative type, and of the four fresh samples of hemangioma, 2 were of proliferative type and 2 degenerative type. SP method results showed that HLA-G was expressed in both proliferative and degenerative hemangioma, but not in normal tissues. The quantum dots double staining exhibited that HLA-G expression was significantly higher in proliferative group than in degenerative (P<0.05) and normal groups (P<0.05), but there was no statistically significant difference between the latter two groups (P>0.05). RT-PCR revealed that HLA-G was transcribed in both the proliferative and degenerative hemangioma tissues, but not in normal tissues. We are led to conclude that the elevated expression of HLA-G in proliferative hemangioma cells may lead to immune tolerance, which allows cells to escape immune surveillance and proliferate. On the other hand, the lower expression of HLA-G in degenerative hemangioma may result in immune cells-induced degeneration of hemangioma.
Journal of Huazhong University of Science and Technology 10/2012; 32(5):713-8. · 0.38 Impact Factor
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ABSTRACT: We previously reported upregulation of aryl hydrocarbon receptor (AhR) expression as a mechanism by which overexpression of Cu/Zn-superoxide dismutase (SOD) and/or catalase accelerates benzo(a)pyrene (BaP) detoxification in mouse aorta endothelial cells (MAECs). The objective of this study was to investigate the regulatory role of specificity protein-1 (Sp1) in AhR expression in MAECs that overexpress Cu/Zn-SOD and/or catalase. Our data demonstrated comparable levels of nuclear Sp1 protein in the transgenic and wild-type MAECs; however, binding of Sp1 protein to the AhR promoter region was more than 2-fold higher in MAECs overexpressing Cu/Zn-SOD and/or catalase than in wild-type cells. Inhibition of Sp1 binding to the AhR promoter by mithramycin A reduced AhR expression and eliminated the differences between wild-type MAECs and three lines of transgenic cells. Functional promoter analysis indicated that AhR promoter activity was significantly higher in MAECs overexpressing catalase than in wild-type cells. Mutation of an AhR promoter Sp1-binding site or addition of hydrogen peroxide to the culture medium reduced AhR promoter activity, and decreased the differences between wild-type MAECs and transgenic cells overexpressing catalase. These results suggest that increased Sp1 binding to the AhR promoter region is an underlying mechanism for upregulation of AhR expression in MAECs that overexpress Cu/Zn-SOD and/or catalase.
Free radical biology & medicine 08/2010; 49(3):487-92. · 5.42 Impact Factor
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ABSTRACT: Telomere-associated proteins function as survival factors in telomere maintenance, which are major contributors to radiosensitivity in human cancers. The aim of this study was to investigate the association of telomere-associated gene expression and radiation resistance in human larynx squamous carcinoma. The changes of telomere-associated gene expressions and bionomical characteristics that occur in two human larynx squamous carcinoma cell lines (Hep-2 and Hep-2R), with different radiosensitivities in vitro were explored in the present study. Based on previous research, elevated POT1 and TPP1 expressions were detected by reverse transcription-PCR and Western blotting in Hep-2R cell lines. Furthermore, Hep-2R cells showed increased recovery ratio accompanied by a reduction of cell arrested in G2/S phase, suggesting that the radioresistance of Hep-2R cells was due to a faster growth in which telomere length had recently been demonstrated to be a powerful prognostic marker. These results manifest that radioresistant Hep-2R cell lines showed certain changes in gene expression and bionomical profiles that are different from the profile changes of the more-sensitive Hep-2 cell lines, and that evaluation of telomere-associated genes may be a prognostic marker for response to radiotherapy in larynx squamous cell carcinoma (LSCC).
Oncology Reports 07/2009; 21(6):1505-9. · 1.84 Impact Factor
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ABSTRACT: Lead is a ubiquitous environmental and industrial pollutant that may have toxic effects on the male. Vitamins may protect against toxic effects of lead in the liver and reproductive system, which is confirmed by our initial research. The aim of this study was to further investigate the protective effects of vitamins (ascorbic acid combined with thiamine) on lead acetate (Pb)-induced reproductive toxicities in mice and study the possible mechanisms underlying these effects. Forty-five male mice were randomly divided into 3 groups, 15 mice in each and received daily intragastric administration with control, Pb (20 mg/kg), and Pb+vitamins (ascorbic acid of 420 mg/kg+thiamine of 30 mg/kg) for 6 weeks, respectively. The Pb-treated animals showed significant decreases in the epididymal sperm count and motility compared to the control group, while the Pb+vitamins group had significant increases for these variables. Moreover, an increasing apoptosis of germinal cells induced by Pb was reduced by vitamin treatment. Pb induced the activation of Caspase-3, Fas/Fas-L and Bcl-2 with elevated levels, and the adaptor protein primarily regulated signaling through Fas and required for Fas-induced apoptosis. In conclusion, ascorbic acid combined with thiamine exhibited protective effect on reproductive system by inhibiting Pb-induced excessive cell apoptosis.
Journal of Huazhong University of Science and Technology 03/2009; 29(1):68-72. · 0.38 Impact Factor
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ABSTRACT: Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical emodin (100, 200 and 400 microg/ml), recombinant human epidermal growth factor (rhEGF, 10 microg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving emodin (400 microg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day 14 wounds than that of vehicle control. The level of transforming growth factor- beta(1) (TGF-beta(1)) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-beta(1) signaling pathway.
European Journal of Pharmacology 08/2007; 567(3):177-85. · 2.52 Impact Factor
