Disease relevance of Ang1

• The adenoviral delivery of Ang1 during the acute phase of myocardial infarction would be feasible to attenuate the progression of cardiac dysfunction in the rat model [1].
• Finally, the elucidation of the protective effect of Ang1 on blood vessel leakiness to plasma proteins raises the possibility of a new strategy for reducing airway edema in inflammatory airway diseases such as asthma and chronic bronchitis [2].
• In contrast, the constitutive expression of Ang1 and Tie2 was not affected during hypoxia or deadaptation [3].
• Neither Ang1 nor Tie1 mRNA or protein showed any significant change at any time point after the infarction [4].
• During sepsis therefore, Ang-1 increases vascular reactivity and has the potential to increase blood pressure and decrease vasopressor requirements in vivo [5].

High impact information on Ang1

• RESULTS: Single local injection of plasmids encoding VEGF165 and Ang1 significantly increased neovascularization and accelerated ulcer healing [6].
• Angiopoietin-1 (Ang1) has potential therapeutic applications in inducing angiogenesis, enhancing endothelial cell survival, and preventing vascular leakage [7].
• The effect of the VEGF/Ang-1 combination on AKT phosphorylation was, instead, additive over time, and sustained over a 24-hour period [8].
• The results showed positive effect of VEGF(165), Ang1 and VEGF(165)+Ang1 on decreasing the myocardial infarct size at the 7th day [9].
• We doubted that these capillaries could do this solely and the potential protective mechanisms of VEGF and Ang1 on myocardium need to be evaluated [9].

Biological context of Ang1

• VEGF increases vascular permeability, but Ang1 has the opposite effect [2].
• Prolonged AAV-mediated Ang1 transgene expression also induced SMC activation, whereas AAV-Ang2 lacked the SMC activating effects and decreased CAV [10].
• We recently reported that Ang1 prevented apoptosis induced by serum deprivation in endothelial cells [11].
• In conclusion, Ang-1 increases vasoconstriction to phenylephrine in the presence of LPS [5].
• RESULTS: Transfection of antisense bFGF ODN (5 mumol.L-1) almost completely inhibited enhanced bFGF mRNA expression and inhibited cell proliferation induced by angiotensin II (Ang 1 mumol.L-1) [12].

Anatomical context of Ang1

• In the early phase postinjury, blood-brain barrier (BBB) breakdown at the lesion site is associated with decreased endothelial Ang1 and increased Ang2 expression, raising the possibility that Ang2 may have a role in early BBB breakdown [13].
• Similar effects at 1 week were evident for Ang1 in glandular epithelium [14].
• The protective effect of VEGF(165) and Ang1 on the myocardium may broaden their functional research and contribute to their clinical use in the future [9].
• As in vitro, the antiapoptosis effect of VEGF(165), Ang1 and VEGF(165)+Ang1 on cardiac myoblasts was observed, which seemed to be related with the activation of phosphatidylinositol-3 kinase and Bcl-2 pathways [9].
• Angiopoietin-1 (Ang1) and Ang2 regulate the maintenance of normal vasculature by direct endothelial and indirect smooth muscle cell (SMC) effects [10].

Associations of Ang1 with chemical compounds

• Neutralizing Ang1 antibody attenuates DETA-NONOate-induced capillary tube formation [15].
• Pretreatment with Ang1 could be beneficial in maintaining normal endothelial cell integrity during intracoronary irradiation or systemic mannitol therapy [11].
• Of interest was the localization of both Ang1 and Ang2 in scattered PAS positive adenohypophysial cells rather than in endothelial cells [16].
• Two phosphatidylinositol 3'-kinase (PI3-kinase)-specific inhibitors, wortmannin and LY294002, blocked the Ang1-induced antiapoptotic effect [11].
• The increased capillary perfusion accompanied by the formation of more stable and mature vessels resistant to fluorescein isothiocyanate-conjugated albumin leakage may serve as in vivo evidence that Ang-1 therapy improves skeletal muscle flap hemodynamics [17].

Other interactions of Ang1

• Angiopoietin-1 (Ang1) is a critical angiogenic factor for vascular maturation and enhances vascular endothelial growth factor (VEGF)-induced angiogenesis in a complementary manner [1].

Analytical, diagnostic and therapeutic context of Ang1

• We hypothesized that gene therapy using Ang1 for AMI might promote angiogenesis cooperatively with intrinsic VEGF, since high concentrations of circulating VEGF have been reported in AMI [1].
• Furthermore, the Ang1 group showed significantly higher cardiac performance in echocardiography (55.0% of ejection fraction, P < 0.05 vs control) than the saline or adenoviral controls (36.0 or 40.5%, respectively) 4 weeks after myocardial infarction [1].
• Ang1 and Tie1 mRNA and protein did not show significant changes after ischaemia/reperfusion [18].
• The ratio of Ang2/Ang1 mRNA and protein in the study group was higher than that in the control group [4].
• CONCLUSIONS: Our findings suggest that the antiinflammatory properties of Ang1 may offer an entirely new therapeutic approach to prevent cardiac allograft arteriosclerosis [19].

References