Ito A, Hirota S, Mizuno H, Kawasaki Y, Takemura T, Nishiura T, Kanakura Y, Katayama Y, Nomura S, Kitamura Y
Department of Pathology, Osaka University Medical School, Suita, Japan.
Pathol Int. 1995 Oct;45(10):715-20. doi: 10.1111/j.1440-1827.1995.tb03387.x.
Edema occurs in some types of chronic inflammation such as nasal polyps, uterine cervical polyps and gastric hyperplastic polyps. However, the factors or cellular components involved in the development of edema in chronic inflammation remain to be clarified. Recently, the gene encoding vascular permeability factor (VPF) or vascular endothelial growth factor (VEGF) and the genes encoding its receptors (kinase insert domain-containing receptor (KDR) and fms-like tyrosine kinase-1 [fit-1]) have been cloned. VPF/VEGF induces vascular hyperpermeability and vascular endothelial proliferation through KDR or fit-1 receptors. As there is a possibility that VPF/VEGF may play a role in the development of edema in chronic inflammation, we examined the messenger (m) RNA expression of VPF/VEGF and its receptors in nasal polyp tissues, which is an example of chronic inflammation with remarkable edema. Using northern blotting, all nasal polyp tissues examined expressed mRNA of VPF/VEGF and KDR. In situ hybridization revealed that VPF/VEGF mRNA-expressing cells were scattered in the edematous stroma of nasal polyps. In the adjacent sections, these cells showed the morphological features of plasma cells and expressed mRNA of immunoglobulin light chains. Human B cell leukemia and plasmacytoma cell lines expressed VPF/VEGF mRNA but human mast-cell leukemia and T cell leukemia cell lines did not. The alternatively spliced pattern of VPF/VEGF transcripts observed in nasal polyp tissues was consistent with that in plasmacytoma cell lines. Taken together, the VPF/VEGF mRNA-expressing cells in nasal polyps appeared to be plasma cells, suggesting that plasma cells may play an important role in the development of edema in chronic inflammation through the production of VPF/VEGF.
水肿发生于某些类型的慢性炎症，如鼻息肉、子宫颈息肉和胃增生性息肉。然而，慢性炎症中水肿形成所涉及的因素或细胞成分仍有待阐明。最近，编码血管通透性因子（VPF）或血管内皮生长因子（VEGF）的基因及其编码受体（含激酶插入结构域受体（KDR）和fms样酪氨酸激酶-1 [fit-1]）的基因已被克隆。VPF/VEGF通过KDR或fit-1受体诱导血管高通透性和血管内皮细胞增殖。由于VPF/VEGF可能在慢性炎症性水肿形成中起作用，我们检测了鼻息肉组织中VPF/VEGF及其受体的信使（m）RNA表达，鼻息肉是伴有明显水肿的慢性炎症的一个例子。采用Northern印迹法，所有检测的鼻息肉组织均表达VPF/VEGF和KDR的mRNA。原位杂交显示，表达VPF/VEGF mRNA的细胞散在于鼻息肉的水肿基质中。在相邻切片中，这些细胞显示出浆细胞的形态特征，并表达免疫球蛋白轻链的mRNA。人B细胞白血病和浆细胞瘤细胞系表达VPF/VEGF mRNA，但人肥大细胞白血病和T细胞白血病细胞系不表达。在鼻息肉组织中观察到的VPF/VEGF转录本的可变剪接模式与浆细胞瘤细胞系中的一致。综上所述，鼻息肉中表达VPF/VEGF mRNA的细胞似乎是浆细胞，提示浆细胞可能通过产生VPF/VEGF在慢性炎症性水肿形成中起重要作用。
