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

血小板衍生生长因子（platelet derived growth factor， PDGF）是多种间充质细胞最有效的分裂原和趋化剂之一。许多研究者报道了IPF和其他肺纤维化患者肺中PDGF的表达增强。为了完成对PDGF活性的调控，我们构建了缺乏细胞内酪氨酸激酶结构域和跨膜部分的PDGF受体β链（XR）胞外结构域的表达质粒，并利用日本血凝病毒(HVJ)-脂质体法估计了经气管转移XR基因对博来霉素诱导的C57BL/6小鼠肺纤维化的治疗作用。XR基因的转移改善了博来霉素诱导的大鼠肺湿重、羟脯氨酸含量和组织病理变化的增加。这些发现提示PDGF在肺纤维化的发病机制中起着至关重要的作用，使用hvj -脂质体方法的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.