Heterogeneity of antigen expression among human umbilical cord vascular endothelial cells: identification of cell subsets by co-expression of haemopoietic antigens

Vermot-Desroches, Claudine; Marchand, Delphine; Roy, Catherine; Wijdenes, John

doi:10.1016/0165-2478(95)02432-8

Cited by 8 publications

(4 citation statements)

References 10 publications

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“…Isolated lin−CD31+CD105+Sca1+CD117+ cells were found to be highly immunoreactive for various established endothelial-cell markers including VE-cadherin (CD144), vascular cell adhesion molecule 1 (VCAM-1, CD106), VEGFR-2, VEGFR-1, CD104 (integrin beta 4), CD34, and for CD14, a marker that is expressed both by hematopoietic cells and by ECs [36]–[39]. No immunoreactivity was detected against hematopoietic lineage markers such as CD45 (leukocyte common antigen), CD11b (macrophage-1 antigen, Mac-1), CXCR4 (chemokine receptor type 4, CD184), F4/80 (a pan macrophage marker), CD115 (macrophage colony-stimulating factor receptor), or against smooth muscle α-actin (Figure 3D).…”

Section: Resultsmentioning

confidence: 99%

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Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell

et al. 2012

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Section: Resultsmentioning

confidence: 99%

“…mRNA expression profile from the isolated ECs corresponds to what is expected from ECs. Note that ECs normally express low levels of various “hematopoietic” markers including CD14 [36]–[39], CD16 [36], and CD45 [38],[65].…”

Section: Supporting Informationmentioning

confidence: 99%

Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell

et al. 2012

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“…Note that "arterial blood-tissue interface" is defined differently from the traditional "blood-tissue interface", i.e. endothelium [ 272 ]. In my model, the term denotes the topological area where blood flow meets surrounding structures, and it includes descriptions such as "basement membrane on which the inner cell lining of vessels rests" or "proteins, glycoproteins and other molecules, including artificial ones, that appeared in fixed positions and form structures in contact with the moving blood.…”

Section: Introductionmentioning

confidence: 99%

Analysis of arterial intimal hyperplasia: review and hypothesis

Субботин

2007

Theor Biol Med Model

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BackgroundDespite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology?HypothesisI argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign" intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates early in life to form a multi-layer intimal hyperplasia and then continues to self-renew in a controlled manner throughout life, relatively rarely compromising the blood supply to the heart, causing complications requiring intervention only in a small fraction of the population, while all humans are carriers of benign hyperplasia. Unfortunately, this fundamental fact has not been widely appreciated in arteriosclerosis research and medical education, which continue to operate on the assumption that the normal arterial intima is always an "ideal" single-layer endothelium. As a result, the disease is perceived and studied as a new pathological event caused by new mechanisms. The discovery that normal coronary arteries are morphologically indistinguishable from deadly coronary arteriosclerosis continues to elicit surprise.ConclusionTwo questions should inform the priorities of our research: (1) what controls switch the single cell-layer intimal phenotype into normal hyperplasia? (2) how is normal (benign) hyperplasia maintained? We would be hard-pressed to gain practical insights without scrutinizing our premises.

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“…However, endothelial cells from large vessels, used most often in those studies, that is primary HUVEC or ECV304 cell line, exhibit important phenotypic and functional differences compared to endothelial cells from microvascular territories where plasma leakage largely occurs [Bender et al, 1994;Mason et al, 1997;Lidington et al, 1999;Murakami et al, 2001;Kieda et al, 2002;Chi et al, 2003]. In particular, primary HUVEC have variable and unstable phenotype [Klein et al, 1995;Vermot-Desroches et al, 1995], whereas the endothelial origin of the large vessel-derived ECV 304 cell line is highly controversial thus questioning its relevance as endothelial cell model [Brown et al, 2000;Drexler et al, 2002]. In this regard, those large vessels-derived endothelial cells appear poorly relevant to the pathophysiology of dengue shock syndrome.…”

Section: Introductionmentioning

confidence: 99%

Dengue virus infection of human microvascular endothelial cells from different vascular beds promotes both common and specific functional changes

et al. 2005

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Dengue shock syndrome (DSS), the major life threatening outcome of severe dengue disease, which occurs in some patients in the course of dengue infection, is the consequence of plasma leakage in the microvascular territories. Data from clinical and in vitro studies suggest that an inadequate immunological response is partly responsible for the pathophysiology of DSS, but few is known concerning the consequences of direct infection of endothelial cells by dengue virus per se. In this study, an attempt was made to study the response of two microvascular human cell lines originating, respectively, from liver and dermis to infection by a dengue type 2 virus, by analyzing the virus-induced modulation of functional markers. It is shown that the two microvascular cell lines exhibit both common and specific behaviors upon infection. In particular, LSEC and HMEC-1 replicate efficiently the low-passage virus and respond to infection by over-producing inflammatory mediators involved in the cross talk with circulating immune cells. However, direct infection modulates differently the cell surface expression of molecules critically involved in the interactions between endothelial and inflammatory cells. ICAM-1 and HLA-I are up regulated as a consequence of infection in LSEC whereas direct infection results in downregulation of ICAM-1 in HMEC-1. The present results show that infection of human microvascular cells by unadapted dengue virus results in both common and specific activation patterns depending likely on the tissue origin of the cells, thus suggesting that endothelia from different territories may contribute differently to the pathophysiological events in the course of dengue infection.

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Heterogeneity of antigen expression among human umbilical cord vascular endothelial cells: identification of cell subsets by co-expression of haemopoietic antigens

Cited by 8 publications

References 10 publications

Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell

Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell

Analysis of arterial intimal hyperplasia: review and hypothesis

Dengue virus infection of human microvascular endothelial cells from different vascular beds promotes both common and specific functional changes

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