Decreased prostaglandin E2 synthesis by lung fibroblasts isolated from rats with bleomycin‐induced lung fibrosis
Decreased prostaglandin E2 synthesis by lung fibroblasts isolated from rats with bleomycin‐induced lung fibrosis
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博莱霉素诱导肺纤维化大鼠肺成纤维细胞的前列腺素 E2 合成减少
DOI：
10.1046/j.1365-2613.1999.00096.x
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发表时间：
1999
影响因子：
3
通讯作者：
S. Sone
中科院分区：
文献类型：
--
作者：
F. Ogushi;T. Endo;K. Tani;Kanji Asada;T. Kawano;H. Tada;K. Maniwa;S. Sone
为了阐明肺纤维化的机制，我们检测了博莱霉素（BLM）诱导的肺纤维化中肺成纤维细胞的功能变化。经过 BLM 或盐水气管内处理后，从大鼠肺部获得肺成纤维细胞。通过 3H-TdR 掺入和直接细胞计数估计，BLM 处理的大鼠成纤维细胞 (BRF) 的自发增殖明显快于生理盐水处理的大鼠成纤维细胞 (NRF)。接下来，我们研究了 BRF 和 NRF 在有或没有白细胞介素 (IL)-1α 刺激的情况下合成前列腺素 (PG) E2，发现 BRF 产生的 PGE2 明显少于 NRF。 BRF和NRF之间的环氧合酶（COX）活性和COX-2 mRNA水平没有显着差异，表明PGE2产量的变化与COX无关，COX是PGE2生产的限速酶。这些结果表明，成纤维细胞的增殖受到正常肺中以自分泌方式释放的 PGE2 的下调，因此在 BLM 诱导的肺纤维化大鼠的肺成纤维细胞中观察到的 PGE2 产生减少可能导致该疾病中成纤维细胞过度增殖。总的来说，这些发现为 BLM 诱导的肺纤维化的发展机制提供了一些线索。
In order to clarify the mechanism of pulmonary fibrosis, we examined the functional changes of lung fibroblasts in bleomycin (BLM)‐induced pulmonary fibrosis. Lung fibroblastic cells were obtained from rat lungs after an intratracheal treatment of BLM or saline. The spontaneous proliferation of BLM‐treated rat fibroblasts (BRF), which was estimated by 3H‐TdR incorporation and direct cell counting, was significantly more rapid than that of normal saline‐treated rat fibroblasts (NRF). Next, we investigated prostaglandin (PG) E2 synthesis by BRF and NRF, with or without stimulation by interleukin (IL)‐1α, and found that PGE2 production by BRF was significantly less than that by NRF. There was no significant difference in cyclooxygenase (COX) activity and COX‐2 mRNA level between BRF and NRF, indicating that the change in PGE2 production was independent of COX, a rate‐limiting enzyme for the production of PGE2. These results suggest that the proliferation of fibroblasts is down‐regulated by PGE2 released from themselves in normal lungs in an autocrine fashion, thus the decreased PGE2 production observed in lung fibroblasts from rats with BLM‐induced pulmonary fibrosis may result in the excessive fibroblast proliferation in this disorder. Overall, these findings throw some light on the mechanism of development of BLM‐induced pulmonary fibrosis.
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DOI：
10.1073/pnas.88.7.2692
发表时间：
1991-04-01
影响因子：
11.1
作者：
XIE, WL;CHIPMAN, JG;SIMMONS, DL
通讯作者：
SIMMONS, DL
前列腺素 E1 对人胎肺成纤维细胞胶原蛋白生成和降解的影响。
影响因子：
3.9
作者：
Barile,FA;Ripley-Rouzier,C;Siddiqi,ZE;Bienkowski,RS
通讯作者：
Bienkowski,RS
DOI：
10.1164/ajrccm/138.3.652
发表时间：
1988-09-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
ELIAS, JA
通讯作者：
ELIAS, JA
DOI：
10.1164/ajrccm/138.3.703
发表时间：
1988-09-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
RAGHU, G;CHEN, YC;RABINOVITCH, PS
通讯作者：
RABINOVITCH, PS
DOI：
10.1164/arrd.1985.131.1.94
发表时间：
2015-05
期刊：
The American review of respiratory disease
影响因子：
--
作者：
J. Elias;M. Rossman;R. Zurier;R. Daniele
通讯作者：
J. Elias;M. Rossman;R. Zurier;R. Daniele