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首页> 外文期刊>Cytokine >Regulation of transforming growth factor-beta secretion by human peritoneal mesothelial and ovarian carcinoma cells.
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Regulation of transforming growth factor-beta secretion by human peritoneal mesothelial and ovarian carcinoma cells.

机译：人腹膜间皮和卵巢癌细胞对转化生长因子-β分泌的调节。

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This study was conducted to compare the secretion of TGF-beta isoforms by human ovarian carcinoma (OVCA) cell lines (n=12) and human peritoneal mesothelial cells (HPMC;n=6) and to examine the regulation of their production by inflammatory cytokines. TGF-beta isoforms were furthermore analysed in OVCA-associated ascitic fluids. HPMC constitutively produced considerable amounts of TGF-beta1 (median 42 pg/10(5)cells; range 7-98) but only minimal amounts of TGF-beta2 (median 0.8 pg/10(5)cells; range 0-1.5). Treatment of HPMC with IL-1beta (10 ng/ml) resulted in a significant elevation of the secretion of both TGF-beta1 (median 187 pg/10(5)cells; range 71-264;P<0.001) and TGF-beta2 (median 1.8 pg/10(5)cells; range 0-13;P<0.01). In OVCA TGF-beta1 and TGF-beta2 were detected in 7/12 and 11/12 of the cell lines, respectively. The levels detected varied widely for TGF-beta1 (median 25 pg/10(5)cells; range 0-410) as well as for TGF-beta2 (median 14 pg/10(5)cells; range 0-419) and there was no correlation between the two isoforms. In contrast to HPMC, TGF-beta secretion by OVCA was not affected by any of the inflammatory cytokines tested. TGF-beta3 could not be detected in supernatants, neither in OVCA nor in HPMC. In ascitic fluids the median level of TGF-beta1 (median 5443 pg/ml; range 737-14687) was 10-fold higher than the level of TGF-beta2 (median 545 pg/ml; range 172-3537). The present data provide a model for the analysis of the molecular mechanisms of aberrant TGF-beta production by OVCA and support the hypothesis that HPMC are an important source of ascitic TGF-beta. Copyright 2000 Academic Press.
机译：进行这项研究的目的是比较人卵巢癌（OVCA）细胞系（n = 12）和人腹膜间皮细胞（HPMC; n = 6）分泌的TGF-β同工型，并研究炎症细胞因子对其产生的调节作用。在OVCA相关的腹水中进一步分析了TGF-β同工型。 HPMC组成性地产生了大量的TGF-beta1（中值42 pg / 10（5）个细胞;范围7-98），但仅产生少量的TGF-beta2（中值0.8 pg / 10（5）个细胞;范围0-1.5）。用IL-1beta（10 ng / ml）处理HPMC导致TGF-beta1（中位187 pg / 10（5）细胞;范围71-264; P <0.001）和TGF-beta2的分泌显着增加（中位数1.8 pg / 10（5）电池;范围0-13; P <0.01）。在OVCA中，分别在7/12和11/12细胞系中检测到TGF-beta1和TGF-beta2。对于TGF-beta1（中值25 pg / 10（5）细胞;范围0-410）以及TGF-beta2（中值14 pg / 10（5）细胞;范围0-419），检测到的水平差异很大两种同工型之间没有相关性。与HPMC相反，OVCA分泌的TGF-β不受任何测试的炎性细胞因子的影响。在OVCA和HPMC中均未在上清液中检测到TGF-β3。在腹水中，TGF-β1（中位数5443 pg / ml;范围737-14687）的中值比TGF-beta2（中位数545 pg / ml;范围172-3537）高10倍。本数据提供了一个模型，用于分析OVCA异常产生TGF-β的分子机制，并支持以下假设：HPMC是腹水TGF-β的重要来源。版权所有2000学术出版社。

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