Wang Yan, Qi Fazhi, Gu Jianying
Shanghai, China From the Department of Surgery, Cancer Hospital of Fudan University, and the Department of Plastic Surgery, Zhongshan Hospital, Fudan University.
Plast Reconstr Surg. 2009 May;123(5):1419-1430. doi: 10.1097/PRS.0b013e3181a073eb.
Intramuscular venous malformation is characterized by abnormal morphology of blood vessels. In certain cases, it displays an invasion of surrounding tissues. The in vitro model of its endothelial cell culture has not been reported, and the pathogenesis of its development is not clear. Matrix metalloproteinase-9 is identified to facilitate cell migration and tumor progression. The aim of this study was to establish the primary cell culture from intramuscular venous malformation and explore its invasive mechanism related to matrix metalloproteinase-9.
Explant culture was adopted to isolate endothelial cells from intramuscular venous malformation. In contrast, with human umbilical vein endothelial cells collected by collagenase digestion, the biological behavior of cell migration and invasion was explored. Western blot, reverse-transcription polymerase chain reaction, and immunohistochemical study were performed to measure matrix metalloproteinase-9 expression of endothelial cells or tissue sections.
The primary endothelial cell culture from intramuscular venous malformation was established successfully by using explant culture. Compared with human umbilical vein endothelial cells, the established endothelial cells indicated more powerful capability of migration and invasion and expressed more matrix metalloproteinase-9 at both mRNA and protein levels. Matrix metalloproteinase-9 mRNA expression in intramuscular venous malformation was significantly higher than in normal subcutaneous tissues. The intensity of matrix metalloproteinase-9 demonstrated no statistically significant differences with varying courses, locations, dimensions, and infiltration degrees.
The positive expression of matrix metalloproteinase-9 of intramuscular venous malformation tissues and endothelial cells provided circumstantial evidence that it may be involved in the pathogenesis of invasive biological behavior of the lesions.
肌内静脉畸形的特征是血管形态异常。在某些情况下，它表现出对周围组织的侵袭。其内皮细胞培养的体外模型尚未见报道，其发病机制也不清楚。已确定基质金属蛋白酶-9促进细胞迁移和肿瘤进展。本研究的目的是建立肌内静脉畸形的原代细胞培养，并探讨其与基质金属蛋白酶-9相关的侵袭机制。
采用组织块培养法从肌内静脉畸形中分离内皮细胞。相比之下，用胶原酶消化收集人脐静脉内皮细胞，探讨细胞迁移和侵袭的生物学行为。进行蛋白质免疫印迹、逆转录聚合酶链反应和免疫组织化学研究，以检测内皮细胞或组织切片中基质金属蛋白酶-9的表达。
采用组织块培养法成功建立了肌内静脉畸形的原代内皮细胞培养。与人类脐静脉内皮细胞相比，所建立的内皮细胞显示出更强的迁移和侵袭能力，并且在mRNA和蛋白质水平上表达更多的基质金属蛋白酶-9。肌内静脉畸形中基质金属蛋白酶-9的mRNA表达明显高于正常皮下组织。基质金属蛋白酶-9的表达强度在病程、位置、大小和浸润程度不同时无统计学显著差异。
肌内静脉畸形组织和内皮细胞中基质金属蛋白酶-9的阳性表达提供了间接证据，表明其可能参与病变侵袭性生物学行为的发病机制。
