Background Postnatal endothelial progenitor cells (EPCs) have been successfully isolated from

Background Postnatal endothelial progenitor cells (EPCs) have been successfully isolated from whole bone marrow blood and the walls of conduit vessels. lymph vessels. Mouse lung microvascular endothelial cells (MLMVECs) were isolated by selection of CD31+ cells. Whereas the majority of the CD31+ cells did not divide some scattered cells started to proliferate giving rise to large colonies (> 3000 cells/colony). Rabbit polyclonal to ZNF490. These highly dividing cells possess the capacity to integrate into various types of vessels including blood and lymph vessels unveiling the presence of local microvascular endothelial progenitor cells (LMEPCs) in adult mouse lung. EPCs could be amplified > passage 30 and still expressed panendothelial markers as well as the progenitor cell antigens but not antigens for immune cells and hematopoietic stem cells. A high percentage of these cells are also positive for Lyve1 Prox1 podoplanin and VEGFR-3 indicating that a considerabe fraction of the cells are committed to develop lymphatic endothelium. Clonogenic highly proliferating cells from limiting dilution assays were also bipotent. Combined in vitro and in vivo spheroid and matrigel assays revealed that these EPCs exhibit vasculogenic capacity by forming functional blood and lymph vessels. Conclusion The lung contains large numbers of EPCs that display commitment for both types Baicalin of vessels suggesting that lung blood Baicalin and lymphatic endothelial cells are derived from a single progenitor cell. Background In the developing embryo blood vessels and later also lymphatic vessels are formed via an initial process of vasculogenesis. This is followed by sprouting and intussusceptive growth of the vessels termed angiogenesis for blood vessels and lymphangiogenesis for lymph vessels. These mechanisms give rise to a complete blood and lymphvascular system consisting of arteries veins capillaries and collectors. Endothelial cells (ECs) are specified according to the circulatory system (blood versus lymph) and to the vessel type (vein artery capillary) to which they belong [1]. However ECs from diseased tissues can have different molecular markers and characteristics from those found in normal vascular beds [2 3 The interface formed by ECs between blood or lymph and the surrounding tissue has different physiological functions in different organs and is an important attribute for tissue homeostasis. Although differentiated endothelium hardly proliferates in most organs under pathological conditions and in female reproductive organs ECs are replaced and proliferate to support tissue growth and to preserve vascular and organ homeostasis [4 5 Already in the 1970s the Baicalin presence of fast-growing endothelial cells within niches of the vessel intima was postulated [6]. These early findings together with more recent data suggest that the turnover rate of ECs in conduit blood vessels in vivo is usually in the range of several years [4 7 Heterogeneity of endothelial cells does not only exist with regard to blood and lymphatic vessels but also along the arterial-capillary-venule axis and between capillaries of specific tissues and organs [4 5 Physiological Baicalin capillary growth can achieve high rates for example cyclically capillary growth is found in the Baicalin corpus luteum to transport blood to the granulosa cells during the menstrual cycle [8]. Thereby the proliferation rate of ECs is comparable in its extent to fast growing tumours [9]. Therefore at least some microvascular ECs and ECs in specific niches possess high endogenous proliferation capacities in vivo as well as high angiogenic potential as part of their physiological role. Under in vitro conditions both microvascular and macrovascular ECs can reestablish their proliferative phenotype but it has been shown that for example pulmonary microvascular ECs from rats grow approximately twice as fast as pulmonary artery ECs [10 11 At the molecular level microvascular ECs possess higher expression of cell cycle regulating genes Baicalin and inactivation of antimitogenic proteins [12]. Based on these results it is not clear whether all microvascular ECs exhibit a higher proliferation rate or whether only a subpopulation of replication-competent cells as suggested.