Browsing by Subject "Vasculogenesis"

Now showing 1 - 5 of 5
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    CCM2 and CCM3 proteins contribute to vasculogenesis and angiogenesis in human placenta
    (Murcia : F. Hernández, 2009) Tanriover, Gamze; Seval, Yasemin; Sati, Leyla; Gunel, Murat; Demir, Necdet
    Placenta as an ideal model to study angiogenic mechanisms have been established in previous studies. There are two processes, vasculogenesis and angiogenesis, involved in blood vessel formation during placental development. Therefore, blood vessel formation is a crucial issue that might cause vascular malformations. One of the vascular malformations is cerebral cavernous malformation (CCM) in the central nervous system, consisting of endothelium-lined vascular channels without intervening normal brain parenchyma. Three CCM loci have been mapped as Ccm1, Ccm2, Ccm3 genes in CCM. In order to investigate whether CCM proteins participate in blood vessel formation, we report here the expression patterns of CCM2 and CCM3 in developing and term human placenta by means of immunohistochemistry and Western blot analysis. CCM2 and CCM3 were obviously detected in the vascular endothelium during early pregnancy. Moreover, vascular endothelium of stem villi revealed a moderate immunostaining for CCM2 and, to a lesser extent, in the endothelium of mature intermediate villi in term placenta. Interestingly, CCM3 immunostaining was weakly localized in the endothelium of mature intermediate villi and showed lesser expression going toward stem villi in term placenta. The expression patterns of the proteins were clearly identified in the vascular endothelium of human placenta, suggesting that they might play roles during angiogenesis and vasculogenesis. Furthermore, with this study, CCM2 and CCM3 have been described for the first time in the human placenta.
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    Morphofunctional basis of the different types of angiogenesis and formation of postnatal angiogenesis-related secondary structures
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Díaz Flores, L.; Gutierrez, R.; García Suárez, M.P.; Sáez, F.J.; Gutiérrez, E.; Valladares, F.; Carrascosa, J.L.; Díaz Flores Jr, L.; Madrid Cuevas, Juan Francisco
    We review the morpho-functional basis of the different types of angiogenesis and report our observations, including the formation of angiogenesisrelated secondary structures. First of all, we consider the following issues: a) conceptual differences between angiogenesis and vasculogenesis, b) incidence of angiogenesis in pre- and postnatal life, c) regions of vascular tree with angiogenic capacity, d) cells (endothelial cells, pericytes, CD34+ adventitial stromal cells of the microvasculature and inflammatory cells) and extracellular matrix components involved in angiogenesis, e) events associated with angiogenesis, f) different types of angiogenesis, including sprouting and intussusceptive angiogenesis, and other angiogenic or vascularization forms arising from endothelial precursor cells (postnatal vasculogenesis), vasculogenesis mimicry, vessel co-option and piecemeal angiogenesis. Subsequently, we consider the specific morphofunctional characteristics of each type of angiogenesis. In sprouting angiogenesis, we grouped the events in three phases: a) activation phase, which includes vasodilation and increased permeability, EC, pericyte and CD34+ adventitial stromal cell activation, and recruitment and activation of inflammatory cells, b)sprouting phase, encompassing EC migration (concept and characteristics of endothelial tip cells, tip cell selection, lateral inhibition, localized filopodia formation, basal lamina degradation and extracellular changes facilitating EC migration), EC proliferation (concept of endothelial stalk cells), pericyte mobilization, proliferation, recruitment and changes in CD34+ adventitial stromal cells and inflammatory cells, tubulogenesis, formation of a new basal lamina, and vascular anastomosis with capillary loop formation, and c) vascular remodelling and stabilization phase (concept of phalanx cells). Subsequently, the concept, incidence, events and mechanisms are considered in the other forms of angiogenesis. Finally, we contribute the formation of postnatal angiogenesis-related secondary structures: a) intravascular structures through piecemeal angiogenesis, including intravascular papillae in vessel tumours and pseudotumours (intravascular papillary endothelial hyperplasia, vascular transformation of the sinus in lymph nodes, papillary intralymphatic angioendothelioma or Dabska tumour, retiform hemangioendothelioma, hemangiosarcoma and lymphangiosarcoma), vascular septa in hemorrhoidal veins and intravascular projections in some tumours; b) arterial intimal thickening; c) intravascular tumours and pseudotumours (e.g. intravenous pyogenic granulomas and intravascular myopericytoma); d) vascular glomeruloid proliferations; and e) pseudopalisading necrosis in glioblastoma multiform.
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    Murine embryonic stem cell in vitro differentiation: applications to the study of vascular development
    (Murcia : F. Hernández, 2003) Feraud, O.; Vittet, D.
    The present review summarizes knowledge accumulated during the last decade concerning in vitro endothelial differentiation from embryonic stem (ES) cells. There is now growing evidence that ES cells may provide a powerful model system to determine the cellular and molecular mechanisms of vascular development. ES cells differentiate into the endothelial lineage by successive maturation steps recapitulating in vivo events observed in the embryo. Further maturation of ES-derived embryoid bodies either in three dimensional gels or in confrontation cultures with tumor spheroids can also provide a model of physiological or tumoral angiogenesis. The data obtained from experimental in vitro differentiation of genetically modified mouse ES cells highlight the potential and the complementarity of this model system to in vivo gene knock out studies. We also consider and discuss some of the potential applications of ES cell technology in vascular biology for future directions in basic research and medicine, by manipulation of differentiation and the generation of cell populations for analysis and transplantation for therapeutic use.
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    Vascular mimicry in glioblastoma following anti-angiogenic and anti-20-HETE therapies
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Angara, Kartik; Rashid, Mohammad H.; Shankar, Adarsh; Ara, Roxan; Iskander, Asm; Borin, Thaiz F.; Jain, Meenu; Achyut, Bhagelu R.; Arbab, Ali S.
    Glioblastoma (GBM) is one hypervascular and hypoxic tumor known among solid tumors. Antiangiogenic therapeutics (AATs) have been tested as an adjuvant to normalize blood vessels and control abnormal vasculature. Evidence of relapse exemplified in the progressive tumor growth following AAT reflects development of resistance to AATs. Here, we identified that GBM following AAT (Vatalanib) acquired an alternate mechanism to support tumor growth, called vascular mimicry (VM). We observed that Vatalanib induced VM vessels are positive for periodic acid-Schiff (PAS) matrix but devoid of any endothelium on the inner side and lined by tumor cells on the outer-side. The PAS+ matrix is positive for basal laminae (laminin) indicating vascular structures. Vatalanib treated GBM displayed various stages of VM such as initiation (mosaic), sustenance, and full-blown VM. Mature VM structures contain red blood cells (RBC) and bear semblance to the functional blood vessel-like structures, which provide all growth factors to favor tumor growth. Vatalanib treatment significantly increased VM especially in the core of the tumor, where HIF-1α was highly expressed in tumor cells. VM vessels correlate with hypoxia and are characterized by co-localized MHC-1+ tumor and HIF-1α expression. Interestingly, 20-HETE synthesis inhibitor HET0016 significantly decreased GBM tumors through decreasing VM structures both at the core and at periphery of the tumors. In summary, AAT induced resistance characterized by VM is an alternative mechanism adopted by tumors to make functional vessels by transdifferentiation of tumor cells into endothelial-like cells to supply nutrients in the event of hypoxia. AAT induced VM is a potential therapeutic target of the novel formulation of HET0016. Our present study suggests that HET0016 has a potential to target therapeutic resistance and can be combined with other antitumor agents in preclinical and clinical trials.
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    Vascular wall-resident stem cells
    (Murcia : F. Hernández, 2010) Klein, Diana; Hohn. Hans-Peter; Kleff, Veronika; Tilki, Derya; Ergün, Süleyman
    New vessels in the adult have been considered to be formed not only by angiogenesis, but also by postnatal vasculogenesis via endothelial progenitor cells (EPCs). However, it is still a matter of debate as to what extent the EPCs contribute to new vessel formation in the adult. While the role of the circulating and bone marrow-derived EPCs has intensively been studied, the contribution of the vascular wall itself was neglected for a long time. Evidence published in the last few years strongly suggests the existence of different stem and progenitor cell types in the vascular wall. Particularly, the presence of EPCs and smooth muscle progenitor cells (SMPCs) in distinct zones of the vascular wall supports the hypothesis that not only BM- or C-EPCs, but also vascular wall-resident stem cells (VW-SCs) might contribute to new vessel formation and vascular wall morphogenesis. However, the differentiation potential of the VW-SCs, e.g. whether a VW-SC is able to give rise to a complete hierarchy of vascular progenitors still remains to be studied. This review will provide a survey about the VW-SCs and their potential impact in vascular biology