Kriehuber E, Breiteneder-Geleff S, Groeger M, Soleiman A, Schoppmann S F, Stingl G, Kerjaschki D, Maurer D
Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, University of Vienna Medical School, Austria.
J Exp Med. 2001 Sep 17;194(6):797-808. doi: 10.1084/jem.194.6.797.
A plexus of lymphatic vessels guides interstitial fluid, passenger leukocytes, and tumor cells toward regional lymph nodes. Microvascular endothelial cells (ECs) of lymph channels (LECs) are difficult to distinguish from those of blood vessels (BECs) because both express a similar set of markers, such as CD31, CD34, podocalyxin, von Willebrand factor (vWF), etc. Analysis of the specific properties of LECs was hampered so far by lack of tools to isolate LECs. Recently, the 38-kD mucoprotein podoplanin was found to be expressed by microvascular LECs but not BECs in vivo. Here we isolated for the first time podoplanin(+) LECs and podoplanin(-) BECs from dermal cell suspensions by multicolor flow cytometry. Both EC types were propagated and stably expressed VE-cadherin, CD31, and vWF. Molecules selectively displayed by LECs in vivo, i.e., podoplanin, the hyaluronate receptor LYVE-1, and the vascular endothelial cell growth factor (VEGF)-C receptor, fms-like tyrosine kinase 4 (Flt-4)/VEGFR-3, were strongly expressed by expanded LECs, but not BECs. Conversely, BECs but not LECs expressed VEGF-C. LECs as well as BECs formed junctional contacts with similar molecular composition and ultrastructural features. Nevertheless, the two EC types assembled in vitro in vascular tubes in a strictly homotypic fashion. This EC specialization extends to the secretion of biologically relevant chemotactic factors: LECs, but not BECs, constitutively secrete the CC chemokine receptor (CCR)7 ligand secondary lymphoid tissue chemokine (SLC)/CCL21 at their basal side, while both subsets, upon activation, release macrophage inflammatory protein (MIP)-3alpha/CCL20 apically. These results demonstrate that LECs and BECs constitute stable and specialized EC lineages equipped with the potential to navigate leukocytes and, perhaps also, tumor cells into and out of the tissues.
淋巴管丛将组织液、过路白细胞和肿瘤细胞导向局部淋巴结。淋巴通道的微血管内皮细胞(LECs)很难与血管内皮细胞(BECs)区分开来,因为二者都表达一组相似的标志物,如CD31、CD34、足状黏蛋白、血管性血友病因子(vWF)等。由于缺乏分离LECs的工具,目前对LECs特异性的分析受到阻碍。最近发现,38-kD黏蛋白血小板内皮细胞黏附分子在体内由微血管LECs表达,而不由BECs表达。在此,我们首次通过多色流式细胞术从真皮细胞悬液中分离出血小板内皮细胞黏附分子阳性(podoplanin(+))的LECs和血小板内皮细胞黏附分子阴性(podoplanin(-))的BECs。两种内皮细胞类型均得以增殖,并稳定表达血管内皮钙黏蛋白、CD31和vWF。LECs在体内选择性表达的分子,即血小板内皮细胞黏附分子、透明质酸受体淋巴管内皮细胞受体-1(LYVE-1)和血管内皮生长因子(VEGF)-C受体、类fms酪氨酸激酶4(Flt-4)/血管内皮生长因子受体-3(VEGFR-3),在扩增的LECs中强烈表达,而在BECs中不表达。相反,BECs表达VEGF-C,而LECs不表达。LECs和BECs都形成具有相似分子组成和超微结构特征的连接接触。然而,这两种内皮细胞类型在体外以严格的同型方式组装成血管管。这种内皮细胞特化延伸到生物学相关趋化因子的分泌:LECs,但不是BECs,在其基底侧组成性分泌CC趋化因子受体(CCR)7配体二级淋巴组织趋化因子(SLC)/CCL21,而两个亚群在激活后,在顶端释放巨噬细胞炎性蛋白(MIP)-3α/CCL20。这些结果表明,LECs和BECs构成稳定且特化的内皮细胞谱系,具备引导白细胞以及或许还有肿瘤细胞进出组织的潜力。