The effects of ceruloplasmin in PI3K/PTEN cell signaling pathway change induced by silica / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the roles of ceruloplasmin (Cp) in PI3K/PTEN cell signaling pathway change in human embryonic lung fibroblasts (HELFs) induced by silica.</p><p><b>METHODS</b>HELFs transfected with pGenesil1.1 plasmid and pGenesil1.1 with PTEN shRNA (PT) plasmid were successfully established. 100 µg/ml silica and different concentrations of Cp (10, 20, 30 µg/ml) were used in this experiment and Cp were treated cells after exposed to silica for 1h. Three different cell lines (including HELFs, PT and cells were transfected with p85 dominant negative mutant plasmid (DN-p85)) were divided into control groups, silica groups and silica+different concentrations of Cp groups. MTT assay was used to detect the effects of Cp on silica-induced cell proliferation after inhibiting PTEN and p85. When suppressing the expression of PTEN and p85, western blot assay was performed to detect the levels of p85, p110, AKT308, AKT473 and ERK, JNK and their phosphorylated levels.</p><p><b>RESULTS</b>After inhibition of PTEN, the high levels of p85 induced by 100 µg/ml silica with 30 µg/ml Cp were markedly decreased (P<0.05). When suppressing p85, the increased cell proliferation was not observed. And the high levels of AKT308, AKT473, ERK and phosphorylated JNK and ERK stimulated by 100 µg/ml silica with 30 µg/ml Cp were decrease (P < 0.05).</p><p><b>CONCLUSION</b>Cp could further strengthened silica-induced cell proliferation by PI3K/AKT/MAPK cell signaling pathway, of which the level of p85 was regulated by PTEN.</p>

Study on the silica-induced cytotoxicity and hprt gene mutagenisis in rat lung fibroblasts and alveolar type II epithelial cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the differences of the silica-induced inhibition on cellular proliferation and hprt gene mutagenesis between lung fibroblasts and alveolar type II cells.</p><p><b>METHODS</b>The proliferation inhibitive cytotoxicity was detected by MTT (3-[4,5-Dimethylthiazolzyl]-2,5-Diphenyl Tetrazolium Bromide) colorimetric method. Mutation in the hprt gene was screened by culture in the presence of the toxic purine analog, 6-thioguanine (6-TG).</p><p><b>RESULTS</b>Under the same circumstances of silica exposure, alveolar type II cells was more sensitive than lung fibroblasts for proliferation inhibition. The median proliferation inhibition concentration (IC50) of silica on epithelial was 140 micrograms/cm2, whereas IC50 of silica on fibroblasts was 282 micrograms/cm2. At the same doses of silica, the hprt gene mutation frequency in type II cells (84.2 x 10(-6))-156.6 x 10(-6) was statistically higher than that in fibroblasts (67.6 x 10(-6)-114.3 x 10(-6), P < 0.05).</p><p><b>CONCLUSION</b>There were significant differences of both silica-induced cell proliferation inhibition and hprt gene mutation between rat lung fibroblasts and type II epithelial cells. In vitro, cultured rat alveolar type II cells were more sensitive in cytotoxicity and hprt gene mutagenesis to silica dust than lung fibroblasts were.</p>

Experimental and Clinical Research for a Collagen-Coated Dacron Graft / 中华胸心血管外科杂志

No interstitial bleeding occurred in either type of grafts. By gross observation and under light microscopy, a smooth neointima was noticed on the surface of collagen coated grafts 30 and 90 days after implantation. In a series of 4 patients with Marfan's syndrome undergoing replacement of the aortic root, hemorrhage through the interstices of the graft was virtually eliminated. There was no complication in any patient after a follow up of 3 months. This study reveals that collagen-coated dacron grafts were totally impervious to blood during and after implantation. The collagen coating can promoting cell growth and graft healing and does not interfere with the physical properties of the dacron grafts. As a prosthesis of aorta replacement , it may be applied clinically with safety. If it is used as small diameter vascular prosthesis,the long-term patency may be improved.