Endoglin Proteins (ENG)

Human Endoglin (ENG) interaction partners

1. CD105(+) fibroblasts were found to circumscribe epithelia with neuroendocrine differentiation. CAF-derived SFRP1, driven by CD105 signaling, was necessary and sufficient to induce prostate cancer neuroendocrine differentiation in a paracrine manner.

2. Combining radiation and CD105 targeting to address the DNA repair.

3. No correlation was identified between the tumor CD105 (endoglin) expression and survival in CSCC patients treated with radical RT +/- chemotherapy.

4. Recombinant short-endoglin overexpression reduces unilateral ureteral obstruction-induced renal fibrosis. As long endoglin overexpression provokes renal fibrosis we conclude that endoglin-mediated induction of renal fibrosis in this model is dependent on its cytoplasmic domain.

5. endoglin promoted VEGF-induced tip cell formation. Mechanistically, endoglin interacted with VEGF receptor (VEGFR)-2 in a VEGF-dependent manner, which sustained VEGFR2 on the cell surface and prevented its degradation. Endoglin mutants deficient in the ability to interact with VEGFR2 failed to sustain VEGFR2 on the cell surface and to promote VEGF-induced tip cell formation.

6. Endoglin isoforms are differentially upregulated in liver samples of patients with chronic and acute liver injury.

7. Ki67 LI, CD105, and alpha-SMA expression showed significant differences between normal, low-risk oral epithelial dysplasia and high-risk oral epithelial dysplasia. These findings further support that features such as increased basal cell layer hyperplasia, abnormal superficial mitosis, increased nuclear-cytoplasmic ratio, and hyperchromasia could be transformation-relevant dysplastic features.

8. Spindle-shaped gastric cancer stromal cells expressing CD73, CD90 or CD105 are involved in disease progression, and among them, CD105-positive cells are strongly associated with poor prognosis.

9. New results furthermore revealed how Eng affects endothelial cell migration and cell shape control in response to these forces, thereby providing new avenues for our understanding of arteriovenous malformations cause.

10. The ratio of sFlt-1/sEGFR could be used as a novel candidate biochemical marker in monitoring the severity of preterm preeclampsia. sEndoglin and sEGFR may be involved in the pathogenesis of small for gestational age in preterm preelampsia.

11. Increased cord blood soluble endoglin is associated with the development of severe or moderate bronchopulmonary dysplasia in preterm infants with maternal preeclampsia.

12. ENG, ACVRL1, and SMAD4 mutations result in different phenotypes in hereditary hemorrhagic telangiectasia

13. High expression of CD105 is associated with Oral Invasive Carcinomas.

14. The role of CD34 in determining the premalignant nature of ral submucous fibrosis (OSF) could not be ascertained, since all endothelial cells were positive for CD34, whereas CD105 appeared to be more specific as it is associated with hypoxia-induced angiogenesis which is occurring in OSF due to hyalinization suggesting, CD105 to be more specific marker to determine neoangiogenesis in OSF

15. Data show that the extracellular domain of endoglin promotes specific platelet adhesion.

16. ENG mutation carriers were more likely than ACVRL1 mutation carriers to have pAVMs (P < 0.001) or multiple lesions (P = 0.03), and to undergo procedural intervention (P = 0.02). The HHT severity score was significantly higher in ENG than in ACVRL1 (P = 0.02).

17. Increased CD105 expression is associated with disease progression in phyllodes tumors

18. levels of the angiogenesis mediators endoglin, HB-EGF, BMP-9 and FGF-2 in patients with severe sepsis and septic shock; endoglin and HB-EGF could be involved in the host response of sepsis; additional studies are warrant to investigate their role as biomarker or therapeutic targets in sepsis

19. A heterozygous genetic variant, c.704dupC; p.Val236Glyfs*98, was identified in the ENG gene. The variant c.704dupC was not previously described in the HHT Mutations Database

20. Endoglin levels are changed after stroke.

Mouse (Murine) Endoglin (ENG) interaction partners

1. endoglin promoted VEGF-induced tip cell formation. Mechanistically, endoglin interacted with VEGF receptor (VEGFR)-2 in a VEGF-dependent manner, which sustained VEGFR2 on the cell surface and prevented its degradation. Endoglin mutants deficient in the ability to interact with VEGFR2 failed to sustain VEGFR2 on the cell surface and to promote VEGF-induced tip cell formation.

2. Endoglin deficiency in hepatic stellate cell significantly aggravates fibrosis in response to injury in two different murine models of liver fibrosis and increases alpha-SMA and fibronectin expression in vitro.

3. Transplantation of mesenchymal stem cells, when combined with endothelial progenitor cells, accelerate muscle recovery in a mouse model of hind limb ischemia, through an endoglin-dependent mechanism.

4. we cannot rule out a possibility that a long-term chronic exposure (9 months and more) to soluble endoglin alone or combined with other cardiovascular risk factors may contribute to alterations of heart function and structure in Sol-Eng+ mice, which is the topic in our lab in ongoing experiments

5. Data show that concomitant activin receptor-like kinase 1 (Acvrl1) and endoglin (Eng) deficiency synergistically decreases pancreatic neuroendocrine tumor volume.

6. Endoglin is necessary for the pro-angiogenic properties of the cardiosphere-derived cells secretome.

7. systemic DPP4 inhibition restores the impaired mononuclear cell homing in Eng+/- animals post-myocardial infarction, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart

8. results suggest that soluble endoglin modulates inflammatory-related diseases and open new perspectives leading to the development of novel and targeted approaches for the prevention and treatment of cardiovascular diseases

9. Endoglin controls blood vessel diameter through endothelial cell shape changes in response to haemodynamic cues.

10. Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling.

11. Identification of novel regulators of developmental hematopoiesis using Endoglin regulatory elements as molecular probes

12. Endoglin has an important role in VSMC recruitment and blood vessel maturation during angiogenesis.

13. the TGFbeta1 coreceptor Eng selectively regulates expression of multiple transient receptor potential channels in the setting of left or right ventricular pressure overload

14. Endothelial cell-specific endoglin expression in islets of Langerhans is sensitive to VEGF and plays partial roles in driving islet vascular development, however such regulation appears to be distinct to mechanisms required to modulate islet viability and size.

15. Study provides evidence that the expression of endoglin is required for the establishment of uterine receptivity and the decidualization process, which mediate embryo adhesion or the attachment reaction.

16. The changes in CD90 and CD105 expression in the testis and ovary of mice are reported.

17. the altered immune activity of endoglin deficient macrophages could help to explain the higher rate of infectious diseases seen in HHT1 patients.

18. These results demonstrate a requirement for endoglin in descendants of Pax3-expressing vascular cell precursors.

19. The similarities in Eng-/- and Mlc2a-/- embryos suggest that Eng-/- mice may suffer from a primary heart developmental defect and secondary defects in vessel patterning.

20. results of our study provide evidence of endoglin as a valid target for cancer therapy and support further development of plasmid shRNA delivery, which have prolonged antitumor effect, especially in combined schedules