Disease relevance of Eng

• Soluble endoglin contributes to the pathogenesis of preeclampsia [1].
• Endoglin (CD105) is the target gene for the hereditary hemorrhagic telangiectasia type I (HHT1), a dominantly inherited vascular disorder [2].
• METHODS: One, 3 and 5 months after RMR, mean arterial pressure and renal function were measured, animals were sacrificed, renal fibrosis was evaluated quantitatively and the expression of endoglin was assessed by western blot, northern blot and immunohistochemistry [3].
• CONCLUSIONS: The present study demonstrates increased endoglin expression in rats with severe hypertension and renal damage [3].
• Temporal changes in renal endoglin and TGF-beta1 expression following ureteral obstruction in rats [4].

High impact information on Eng

• By surface labeling and immunoprecipitation experiments, we show that endoglin is found in significant amounts exposed at the plasma membrane of HSC and MFB, which is a pivotal prerequisite for binding of and signaling in response to TGF-beta [5].
• Moreover, the determined molecular weight (M(r) 160) and the observed reductant sensitivity after treatment with dithiothreitol resemble those of a closely related type III receptor, endoglin (CD105) [5].
• Furthermore, small interfering RNA-mediated suppression of endoglin or ZRP-1, or clustering of endoglin in endothelial cells, led to mislocalization of F-actin fibers [6].
• Expression of endoglin resulted in a dramatic reorganization of the actin cytoskeleton [6].
• The endoglin interacting region was mapped within the three double zinc finger LIM domains of the ZRP-1 C terminus [6].

Biological context of Eng

• Conversely, we found that TGF-beta binding to endoglin required the presence of receptor type II as evidenced by transient transfections experiments in COS cells [2].
• Both the expression of vascular endothelial growth factor (VEGF) and endoglin (CD105) play a key role in neovascularization and wound healing after soft tissue grafts in irradiated and nonirradiated tissue [7].
• Up-regulation of endoglin, a TGF-beta-binding protein, in rats with experimental renal fibrosis induced by renal mass reduction [3].

Anatomical context of Eng

• Transforming growth factor beta receptor endoglin is expressed in cardiac fibroblasts and modulates profibrogenic actions of angiotensin II [8].
• Endoglin is a component of the transforming growth factor-beta receptor complex abundantly expressed at the surface of endothelial cells and plays an important role in cardiovascular development and vascular remodeling [6].
• In the absence of endoglin, F-actin was localized to dense aggregates of bundles, whereas in the presence of endoglin, expressed in endothelial cells, F-actin was in stress fibers and colocalized with ZRP-1 [6].
• Myoblasts stably transfected with endoglin showed a decrease in the expression of lumican both at the RNA and protein levels [9].
• Western and Northern blot analysis identified the expression of endoglin protein and mRNA transcript in both human and rat mesangial cells [10].

Associations of Eng with chemical compounds

• MAPKp42/44 inhibition attenuated Ang II-induced endoglin expression [8].
• Endoglin is a membrane glycoprotein of the TGF-beta1 receptor system [4].

Regulatory relationships of Eng

• Ang II-induced decrease in MMP-1 protein expression and increase in type I collagen protein expression were both blocked by a specific endoglin antibody [8].

Other interactions of Eng

• Ang II increased the expression of endoglin mRNA and protein in a concentration and time-dependent manner, with no effect on TGF-beta receptors I and II expression [8].
• Role of endoglin in cellular responses to transforming growth factor-beta. A comparative study with betaglycan [2].
• Hypoxia maintained the expression of CD44 (hyaluronan receptor), ALCAM (CD166), and endoglin (transforming growth factor-beta receptor) [11].

Analytical, diagnostic and therapeutic context of Eng

• The presence of endoglin in HSC of rat liver was confirmed by molecular cloning of the endoglin cDNA and immunocytochemistry [5].
• Northern blot analysis also revealed a decreased alpha2 (I) procollagen mRNA expression in endoglin transfectants [12].

References