Endoglin (CD 105) expression in human lymphoid organs and placenta

Dağdevıren, Attıla; Müftüoğlu, Sevda; Çakar, Ayşe Nur; Örs, Ülken

doi:10.1016/s0940-9602(98)80109-x

Cited by 22 publications

(12 citation statements)

References 27 publications

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“…Examination of tonsil and mesenteric lymph nodes showed that endoglin levels are further raised in high endothelial cells associated with T cell extravasation ( Fig. 1 G), in agreement with previous data [43].…”

Section: Endoglin Expression Is Variable In Normal Tissuessupporting

confidence: 92%

Inducible expression of human endoglin during inflammation and wound healing in vivo

et al. 2002

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Section: Endoglin Expression Is Variable In Normal Tissuessupporting

confidence: 92%

Inducible expression of human endoglin during inflammation and wound healing in vivo

et al. 2002

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“…The active role played by endoglin in this process is compatible with: (1) the high expression of endoglin in high endothelial venules, 23 characterized by facilitating circulating lymphocytes to directly enter lymph nodes 36 ; (2) the increased expression of endoglin in endothelia on inflammatory stimuli 21,37 and during neoangiogenesis 5,38 ; and (3) the impaired recruitment of HHT1 mononuclear cells to the ischemic heart in a mouse model. 39 Our results suggest that the mechanism by which endothelial endoglin contributes to leukocyte extravasation involves intercellular adhesion mediated by the RGD motif present on the ectodomain of endoglin.…”

Section: Discussionmentioning

confidence: 79%

“…22 Moreover, arterial, venous, and capillary endothelia in lymphoid organs are highly reactive with anti-endoglin antibodies and a marked staining pattern is observed in high endothelial venules. 23 Although endoglin is present throughout the vascular endothelium, its expression is stronger in capillaries, where most leukocyte infiltration to organs occurs, than in veins or arteries, 24 suggesting a role for endothelial endoglin in lymphocyte trafficking and transmigration. The purpose of this study is to assess this hypothesis.…”

Section: Introductionmentioning

confidence: 99%

Endothelial endoglin is involved in inflammation: role in leukocyte adhesion and transmigration

Rossi

Sanz-Rodrı́guez

Eleno

et al. 2013

Blood

141

152

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Key Points• Endothelial endoglin has a regulatory role in leukocyte trafficking through vascular endothelia.• Leukocytes and endothelial cells interact via integrin receptors and endoglin, being this cell adhesion process stimulated by inflammatory stimuli.Human endoglin is an RGD-containing transmembrane glycoprotein identified in vascular endothelial cells. Although endoglin is essential for angiogenesis and its expression is up-regulated in inflammation and at sites of leukocyte extravasation, its role in leukocyte trafficking is unknown. This function was tested in endoglin heterozygous mice (Eng ؉/؊ ) and their wild-type siblings Eng ؉/؉ treated with carrageenan or LPS as inflammatory agents. Both stimuli showed that inflammation-induced leukocyte transendothelial migration to peritoneum or lungs was significantly lower in Eng ؉/؊ than in Eng ؉/؉ mice. Leukocyte transmigration through cell monolayers of endoglin transfectants was clearly enhanced in the presence of endoglin. Coating transwells with the RGD-containing extracellular domain of endoglin, enhanced leukocyte transmigration, and this increased motility was inhibited by soluble endoglin. Leukocytes stimulated with CXCL12, a chemokine involved in inflammation, strongly adhered to endoglincoated plates and to endoglin-expressing endothelial cells. This endoglin-dependent adhesion was abolished by soluble endoglin, RGD peptides, the anti-integrin ␣5␤1 inhibitory antibody LIA1/2 and the chemokine receptor inhibitor AMD3100. These results demonstrate for the first time that endothelial endoglin interacts with leukocyte integrin ␣5␤1 via its RGD motif, and this adhesion process is stimulated by the inflammatory chemokine CXCL12, suggesting a regulatory role for endoglin in transendothelial leukocyte trafficking. (Blood. 2013;121(2):403-415) IntroductionThe vascular endothelium controls the transit of white blood cells into and out of the bloodstream. The migration of leukocytes involves the adhesive interaction of cell surface receptors with ligands expressed on endothelial cells in a process regulated by inflammatory stimuli. Stromal-derived factor 1 (SDF1␣), renamed CXCL12, is a potent chemoattractant for a variety of cells including lymphocytes, monocytes, dendritic cells, and hematopoietic stem cells. 1 CXCL12 and its receptor CXCR4 play relevant roles in immune and inflammatory responses, including leukocyte migration and recruitment, as well as integrin-dependent adhesion and transendothelial migration. 1 CXCL12 is a critical activator of endothelial progenitors by inducing a proangiogenic phenotype and increasing migration and rolling mediated by ␣4 and ␣M integrin subunits. 2 The process of leukocyte migration through the endothelial cell monolayer involves an interaction between leukocytes' integrins and endothelial-cell receptors, both acting as adhesion molecules. Integrins most relevant to leukocytes belong to the ␤ 1 -integrin and the ␤ 2 -integrin subfamilies. Classic chemoattractants and chemokines are the most powerful physiologic activat...

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“…Recently, it has been proposed that serial determinations of the concentrations of sVEGFR-1 [38,39], PlGF [38], and s-Eng [39] are more informative in assessing the risk for PE than are single measurements in the first or second trimester. This is plausible because PlGF, s-Eng, and sVEGFR-1 are produced by the trophoblast [23,[39][40][41][42][43][44] and, therefore, maternal plasma concentrations can change with placental development from the first to the second trimester.…”

mentioning

confidence: 99%

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

Erez

Romero

Espinoza

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

273

233

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The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age, The Journal of Maternal-Fetal & Neonatal Medicine, 21:5, 279-287, DOI: 10.1080 AbstractIntroduction. An imbalance between angiogenic and anti-angiogenic factors has been proposed as central to the pathophysiology of preeclampsia (PE). Indeed, patients with PE and those delivering small-for-gestational age (SGA) neonates have higher plasma concentrations of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) and the soluble form of endoglin (s-Eng), as well as lower plasma concentrations of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) than do patients with normal pregnancies. Of note, this imbalance has been observed before the clinical presentation of PE or the delivery of an SGA neonate. The objective of this study was to determine if changes in the profile of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters are associated with a high risk for the subsequent development of PE and/or delivery of an SGA neonate. Methods. This longitudinal case-control study included 402 singleton pregnancies in the following groups: (1) normal pregnancies with appropriate for gestational age (AGA) neonates (n ¼ 201); (2) patients who delivered an SGA neonate (n ¼ 145); and (3) patients who developed PE (n ¼ 56). Maternal plasma samples were obtained at the time of each prenatal visit, scheduled at 4-week intervals from the first or early second trimester until delivery. In this study, we included two samples per patient: (1) first sample obtained between 6 and 15 weeks of gestation ('first trimester' sample), and (2) second sample obtained between 20 and 25 weeks of gestation ('second trimester' sample). Plasma concentrations of s-Eng, sVEGFR-1, and PlGF were determined by specific and sensitive immunoassays. Changes in the maternal plasma concentrations of these angiogenesis-related factors were compared among normal patients and those destined to develop PE or deliver an SGA neonate while adjusting for maternal age, nulliparity, and body mass index. General linear models and polytomous logistic regression models were used to relate the analyte concentrations, ratios, and product to the subsequent development of PE and SGA. Results.(1) An increase in the maternal plasma concentration of s-Eng between the first and second trimesters conferred risk for the development of preterm PE and SGA (OR 14.9, 95% CI 4.9-45.0 and OR 2.9, 95% CI 1.5-5.6, respectively).(2) An increase in the maternal plasma concentration of sVEGFR-1 between the first and second trimester conferred risk for the development of preterm PE (OR 3.9, 95% CI 1.2-12.6). (3) A subnormal increase in maternal plasma PlGF concentration between the first and the second trimester was a risk factor for the subsequent development of preterm and term PE (OR 4....

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Endoglin (CD 105) expression in human lymphoid organs and placenta

Cited by 22 publications

References 27 publications

Inducible expression of human endoglin during inflammation and wound healing in vivo

Inducible expression of human endoglin during inflammation and wound healing in vivo

Endothelial endoglin is involved in inflammation: role in leukocyte adhesion and transmigration

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

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