Endoglin is a component of the transforming growth factor-beta receptor system in human endothelial cells.

Cheifetz, Sela; Bellón, Teresa; Calés, Carmela; Vera, Sonia; Bernabéu, Carmelo; Massagué, Joan; Letarte, Michelle

doi:10.1016/s0021-9258(18)41732-2

Cited by 741 publications

(91 citation statements)

References 28 publications

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“…We demonstrated previously that ENG binds TGF‐β1 and TGF‐β3 isoforms in association with TGFBR2 (46) and that Eng ‐/‐ ECs show reduced binding to TGF‐β1 as measured by affinity cross‐linking. ENG alters TGF‐β receptor levels in a very context‐dependent manner and determines the balance between ALK5 (Smad2 and Smad3 mediated) or ALK1 (Smad1, Smad5, and Smad8 mediated) pathways (47).…”

Section: Discussionmentioning

confidence: 81%

Increased endothelial cell permeability in endoglin-deficient cells

Jerkić¹,

Letarte²

2015

The FASEB Journal

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Endoglin (ENG) is a TGF-b superfamily coreceptor essential for vascular endothelium integrity. ENG mutations lead to a vascular dysplasia associated with frequent hemorrhages in multiple organs, whereas ENG null mouse embryos die at midgestation with impaired heart development and leaky vasculature. ENG interacts with several proteins involved in cell adhesion, and we postulated that it regulates vascular permeability. The current study assessed the permeability of ENG homozygous null (Eng 2/2 ), heterozygous (Eng +/2 ), and normal (Eng +/+ ) mouse embryonic endothelial cell (EC) lines. Permeability, measured by passage of fluorescent dextran through EC monolayers, was increased 2.9-and 1.7-fold for Eng 2/2 and Eng +/2 ECs, respectively, compared to control ECs and was not increased by TGF-b1 or VEGF. Prolonged starvation increased Eng 2/2 EC permeability by 3.7-fold with no effect on control ECs; neutrophils transmigrated faster through Eng 2/2 than Eng +/+ monolayers. Using a pull-down assay, we demonstrate that Ras homolog gene family (Rho) A is constitutively active in Eng 2/2 and EngECs. We show that the endothelial barrier destabilizing factor thrombospondin-1 and its receptor-like protein tyrosine phosphatase are increased, whereas stabilizing factors VEGF receptor 2, vascular endothelial-cadherin, p21-activated kinase, and Ras-related C3 botulinum toxin substrate 2 are decreased in Eng 2/2 cells. Our findings indicate that ENG deficiency leads to EC hyperpermeability through constitutive activation of RhoA and destabilization of endothelial barrier function.-Jerkic, M., Letarte, M. Increased endothelial cell permeability in endoglin-deficient cells. FASEB J. 29, 3678-3688 (2015). www.fasebj.org

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Section: Discussionmentioning

confidence: 81%

Increased endothelial cell permeability in endoglin-deficient cells

Jerkić¹,

Letarte²

2015

The FASEB Journal

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“…These cells could be leukocytes, which have been shown to express PECAM-1 (Liao et al 1995). Nestin also co-localized with endoglin, which is a component of the transforming growth factor (TGF)-beta receptor complex (Cheifetz et al 1992). It has been shown that endoglin is expressed on endothelial cells of normal and especially proliferating blood vessels and is implicated in endothelial cell function (Gougos and Letarte 1990; Kumar et al 1996).…”

Section: Discussionmentioning

confidence: 99%

“…These cells varied in staining intensity and had often a stroma-like appearance. It has been reported that, in some tissues, endoglin and CD34 mark not only vascular endothelial cells but also fibroblasts and leukocytes, which could explain the additional occurrence of endoglin-positive/nestin-negative and CD34-positive/nestin-negative cells (Nakayama et al 2000; Balza et al 2001; O'Connell et al 1992). However, it can neither be excluded that a minute number of PECAM-1, CD34, and endoglin-positive endothelial cells of small blood vessels do not express nestin nor that nestin is expressed in a small subpopulation of non-endothelial cells that are also positive for the tested endothelial markers.…”

Section: Discussionmentioning

confidence: 99%

Nestin Is Expressed in Vascular Endothelial Cells in the Adult Human Pancreas

Klein¹,

Ling

Heimberg

et al. 2003

J Histochem Cytochem.

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S U M M A R YIn this study we examined the expression of nestin in islets, the exocrine part, and the big ducts of the adult human pancreas by immunofluorescent double staining. Two different anti-nestin antisera in combination with various pancreatic and endothelial markers were employed. Nestin-immunoreactive cells were found in islets and in the exocrine portion. All nestin-positive cells co-expressed the vascular endothelial markers PE-CAM-1 (CD31), endoglin (CD105), and CD34 as well as vimentin. Endocrine, acinar, and duct cells did not stain for nestin. We also demonstrated that in the area of big pancreatic ducts, nestin-positive cells represent small capillaries scattered in the connective tissue surrounding the duct epithelium and do not reside between the duct cells. We detected nestinexpressing endothelial cells located adjacent to the duct epithelium where endocrine differentiation occurs. We have shown that nestin is expressed by vascular endothelial cells in human pancreas, and therefore it is unlikely that nestin specifically marks a subpopulation of cells representing endocrine progenitors in the adult pancreas.

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“…TGF-β receptor is an important key inducer of EMT-TFs, which changes expression levels of EMT markers in CRC [17,18]. CD105 (endoglin), as a neoangiogenesisrelated protein, is known as a component of TGF-β receptor and a regulator for TGF-β signaling [19]. Studies performed on cancer have reported that CD105 may induce EMT program through EMT-TFs and play a functional role in maintaining cancer stem cells (CSCs) [20,21].…”

Section: Introductionmentioning

confidence: 99%

Expressions of TWIST1 and CD105 markers in colorectal cancer patients and their association with metastatic potential and prognosis

et al. 2021

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Background TWIST1 and CD105, which contribute to tumor malignancy, are overexpressed in cancers. Accordingly, TWIST1 enhances epithelial-to-mesenchymal transition (EMT) and promotes the formation of cancer stem cells (CSCs). Also, CD105 is a neoangiogenesis marker in endothelial cells, which is introduced as a CSC marker in tumoral epithelial cells in several types of cancers. The present study was aimed to investigate expressions of TWIST1 and CD105 in colorectal cancer (CRC) patients. Methods Expressions of TWIST1 and CD105 in 250 CRC tissue samples were evaluated using immunohistochemistry on tissue microarrays (TMAs). In this regard, TWIST1 expression was investigated in the subcellular locations (cytoplasm and nucleus), while CD105 was mapped in endothelial cells and cytoplasmic tumor cells of CRC tissues. The association between the expression of these markers and clinicopathological parameters, as well as survival outcomes were analyzed. Results Results indicate a statistically significant association between higher nuclear expression levels of TWIST1 and distant metastases in CRC (P = 0.040) patients. In addition, it was shown that the increased nuclear expression of TWIST1 had a poor prognostic value for disease-specific survival (DSS) and progression-free survival (PFS) (P = 0.042, P = 0.043, respectively) in patients with CRC. Moreover, analysis of CD105 expression level has revealed that there is a statistically significant association between the increased expression of CD105 in tumoral epithelial cells and more advanced TNM stage (P = 0.050). Conclusions Our results demonstrate that nuclear TWIST1 and cytoplasmic CD105 expressions in tumor cells had associations with more aggressive tumor behavior and more advanced diseases in CRC cases.

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Endoglin is a component of the transforming growth factor-beta receptor system in human endothelial cells.

Cited by 741 publications

References 28 publications

Increased endothelial cell permeability in endoglin-deficient cells

Increased endothelial cell permeability in endoglin-deficient cells

Nestin Is Expressed in Vascular Endothelial Cells in the Adult Human Pancreas

Expressions of TWIST1 and CD105 markers in colorectal cancer patients and their association with metastatic potential and prognosis

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