In vivo transfer of an extracellular domain of platelet-derived growth factor beta gene by HVJ-liposome method ameliorated bleomycin-induced pulmonary fibrosis.

血小板源性生长因子（PDGF）是一种最有效的有丝分裂原和各种间充质细胞的化学引诱剂。许多研究者报告了IPF和其他肺纤维化患者肺中PDGF表达增加。为了实现PDGF活性的调控，我们构建了PDGF受体β链（XR）胞外区的表达质粒，该表达质粒缺乏胞内酪氨酸激酶区和跨膜区，并采用日本血凝病毒（HVJ）-脂质体法评价了经气管导入XR基因对博莱霉素诱导的C57 BL/6小鼠肺纤维化的治疗作用。XR基因的转染改善了博莱霉素引起的肺湿重、羟脯氨酸含量的增加和肺组织病理学改变。提示PDGF在肺纤维化的发病机制中起重要作用，利用HVJ-脂质体法转染XR基因可能限制肺纤维化的进展。

Platelet-derived growth factor (PDGF) is one of the most potent mitogens and chemoattractants for a variety of mesenchymal cells. A number of investigators have reported augmented expression of PDGF in the lung with IPF and other pulmonary fibrosis. To accomplish regulation of PDGF activity, we constructed an expression plasmid of the extracellular domain of PDGF receptor beta chain (XR), which lacks intracellular tyrosine kinase domain and transmembrane portions, and we estimated the therapeutic effects of the XR gene transfer through trachea on bleomycin-induced lung fibrosis of C57BL/6 mice by using hemagglutinating virus of Japan (HVJ)-liposome method. The transfer of the XR gene improved the increase in the wet weight, hydroxyproline content and histopathologic change of the lung that was induced by bleomycin. These findings suggested that PDGF playd a crucial role in the pathogenesis of pulmonary fibrosis, and the XR gene by using the HVJ-liposome method may limit the progression of pulmonary fibrosis.