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源自肺纤维化病变部位的成纤维细胞迁移增强。

Enhanced migration of fibroblasts derived from lungs with fibrotic lesions.

作者信息

Suganuma H, Sato A, Tamura R, Chida K

机构信息

Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.

出版信息

Thorax. 1995 Sep;50(9):984-9. doi: 10.1136/thx.50.9.984.

Abstract

BACKGROUND

The migration and proliferation of fibroblasts may be important in the pathogenesis of pulmonary fibrosis. Considerable data are available on the proliferation of fibroblasts, but very few on their migration.

METHODS

The migratory activity of fibroblasts obtained from lung biopsy specimens from 11 patients with idiopathic pulmonary fibrosis (IPF) was studied using a 96-well chemotaxis chamber. Fibroblasts from eight normal controls, seven patients with interstitial fibrosis associated with a collagen vascular disease (IP-CVD), and 13 patients with sarcoidosis were also examined. Migratory activity was tested in a serum-free medium in the presence and absence of platelet derived growth factor (PDGF), 30 ng/ml, as a chemoattractant.

RESULTS

Migration of fibroblasts from patients with IPF was enhanced in serum-free maintenance medium alone (mean (SD) controls v IPF: 183 (86) v 689 (491) cells/field), and was also enhanced when cells were stimulated by PDGF (controls v IPF: 829 (222) v 1928 (600) cells/field). Fibroblasts from tissues with dense fibrosis had a greater capacity for migration than those from an earlier stage of fibrosis. No correlation was found between migratory activity and proliferative capacity of the individual cells.

CONCLUSIONS

The fact that fibroblasts from fibrotic lungs migrate faster than those from controls suggests that migration is related to the initiation of the pulmonary fibrotic process. These in vitro studies suggest that fibroblasts derived from the lungs of patients with pulmonary fibrosis have a migratory phenotype. Such a change in fibroblast phenotype, if it occurred in vivo, may be important in the context of the pathogenesis of pulmonary fibrosis.

摘要

背景

成纤维细胞的迁移和增殖可能在肺纤维化的发病机制中起重要作用。关于成纤维细胞增殖的资料很多,但关于其迁移的资料却很少。

方法

使用96孔趋化性小室研究了11例特发性肺纤维化(IPF)患者肺活检标本中获得的成纤维细胞的迁移活性。还检测了8名正常对照者、7例与胶原血管疾病相关的间质性纤维化患者(IP-CVD)以及13例结节病患者的成纤维细胞。在有无作为趋化剂的30 ng/ml血小板衍生生长因子(PDGF)存在的无血清培养基中测试迁移活性。

结果

仅在无血清维持培养基中,IPF患者的成纤维细胞迁移就增强了(平均(标准差)对照组与IPF组:183(86)个/视野对689(491)个/视野),当细胞受到PDGF刺激时迁移也增强(对照组与IPF组:829(222)个/视野对1928(600)个/视野)。来自致密纤维化组织的成纤维细胞比纤维化早期组织的成纤维细胞具有更强的迁移能力。未发现单个细胞的迁移活性与增殖能力之间存在相关性。

结论

纤维化肺中的成纤维细胞比对照者的成纤维细胞迁移更快这一事实表明,迁移与肺纤维化过程的起始有关。这些体外研究表明,肺纤维化患者肺中来源的成纤维细胞具有迁移表型。如果这种成纤维细胞表型的变化发生在体内,可能在肺纤维化的发病机制中具有重要意义。

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