Disease relevance of ANG

• Levels of soluble ANG were elevated in RA (351 +/- 25.7 ng/ml, p < 0.001), in RAEB/RAEB-t (402 +/- 17.9 ng/ml; p < 0.001), in CMML (413.8 +/- 29.5 ng/ml; p < 0.001), and in patients with AML (305.1 +/- 17.1 ng/ml; p < 0.01, controls 255.4 +/- 8.1 ng/ml) [1].
• In this study, we examined the regulation of VEGF expression in vascular smooth muscle cells (VSMC) by hyperglycemia as well as by angiotensin II (ANG II) [2].
• We also proved that another tumorigenic androgen receptor-positive prostate cancer cell line, 22Rv1, secretes higher levels of ANG than VEGF [3].
• BACKGOUND: The distribution of angiogenin (ANG) in normal colorectal and colorectal cancer tissues has not been precisely elucidated, while studies on the clinical significance of ANG have been scanty at best [4].
• ANG in RA SF was 248.7 +/- 17.4 ng/ml, which did not differ significantly from levels found in osteoarthritis (OA; 305.9 +/- 23.1 ng/ml) [5].
• Angiogenin is related to worsening heart failure severity (NYHA classification), with the highest levels in NYHA class III [6].

Psychiatry related information on ANG

• The losartan-sensitive sites have been shown to mediate all of the major ANG II-induced biologic effects, including vasoconstriction, aldosterone and catecholamine release, and central, ANG II-induced drinking behavior [7].
• Finally, independent of the level of physical activity, UVNa was negatively correlated with PRA, ANG II, and Aldo [8].
• Significant univariate content scale differences were found for the Anger (ANG) scale with the PTSD group scoring higher [9].

High impact information on ANG

• Aldosterone secretion by glomerulosa cells is stimulated by angiotensin II (ANG II), extracellular K(+), corticotrophin, and several paracrine factors [10].
• Activation of protein kinase C by diacylglycerol (DAG) inhibits aldosterone production, whereas the arachidonate released from DAG in ANG II-stimulated cells is converted by lipoxygenase to 12-hydroxyeicosatetraenoic acid, which may also induce Ca(2+) signaling [10].
• ANG II, bound to AT(1) receptors, acts through the inositol 1,4,5-trisphosphate (IP(3))-Ca(2+)/calmodulin system [10].
• ANG mutations segregate with familial and 'sporadic' amyotrophic lateral sclerosis [11].
• ANG II raises blood pressure by direct vasoconstrictor action on arteriolar muscles in some animals, but perhaps more generally by acting on the nervous system and adrenal paraneurons [12].

Chemical compound and disease context of ANG

• In conclusion, blood pressure responses to ANG II and SNP are altered, and microvascular structural changes prevail in this model of fetal programming of hypertension [13].
• There was no change in proteinuria or 24-h ambulatory blood pressure (BP) with add-on ANG II receptor blockade with losartan therapy [14].
• This study investigated whether low-density lipoprotein (LDL) activates local RAS in cultured human mesangial cells (HMC) and, at the same time, whether ANG II mediates LDL-induced mesangial cell proliferation, hypertrophy, and superoxide (O2-) generation [15].
• PGE2 and PRA concentrations were significantly higher in renal veins of kidneys with arterial stenosis with patients supine and after sitting up for 15 min, but the ANG II concentration was raised only with the patient sitting [16].
• In conclusion, despite elevated plasma levels, the vasoconstrictor influence of ANG II on the coronary circulation in vivo is reduced after myocardial infarction [17].

Biological context of ANG

• 2. Analysis of the angiogenin (ANG) gene in the authors' population has demonstrated a significant allelic association with the rs11701 single nucleotide polymorphism (SNP) and identified a novel mutation in two individuals with sporadic ALS that potentially inhibits angiogenin function [18].
• Surprisingly, Fab binding induces a dramatic conformational change in the cell binding region of ANG at the opposite end of the molecule from the combining site; crosslinking experiments indicate that this rearrangement also occurs in solution [19].
• Circulating plasma sE-selectin (sE-S), sP-selectin (sP-S), human soluble vascular cell adhesion molecule-1 (sVCAM-1), and human soluble intercellular adhesion molecule-1 (sICAM-1) and serum levels of human vascular endothelial growth factor (VEGF), angiogenin (ANG), and placenta growth factor (P/GF) were measured with ELISAs [20].
• Thus, in the present study, hypoxia-induced up-regulation in melanoma cells was only observed for ANG and vascular endothelial growth factor [21].
• Its primary effector hormone, angiotensin II (ANG II), not only mediates immediate physiological effects of vasoconstriction and blood pressure regulation, but is also implicated in inflammation, endothelial dysfunction, atherosclerosis, hypertension, and congestive heart failure [22].

Anatomical context of ANG

• The mainstays of therapy, glycemic control and inhibition of ANG II, are key measures to prevent early podocyte injury and the subsequent development of diabetic nephropathy [23].
• Persistent activation of the ANG/Tie-2 system in addition to high levels of VEGF may keep the vasculature in a destabilized condition and may account for the continuous formation of new and immature blood vessels resulting in massive plasma extravasation and repeated bleeding episodes [24].
• Synovial lining cells, macrophages, endothelial cells, and vascular smooth muscle cells were immunopositive for bFGF and ANG; however, their expression was not up-regulated in RA ST compared to ST from OA and normal subjects [5].
• ANG immunoreactivity was also observed in interstitial cells in the vicinity of and at the invasion front of cancer cells, as well as in normal superficial epithelial cells and in some interstitial cells [4].
• It may be that some of these mediators, like ANG, play a role in the physiology of normal synovium [5].

Associations of ANG with chemical compounds

• We also examined whether the 12-lipoxygenase (12-LO) product 12-hydroxyeicosatetraenoic acid (12-HETE) can alter VEGF expression, since 12-LO products of arachidonic acid have angiogenic properties, and ANG II as well as high glucose (HG, 25 mM) can increase 12-LO activity and expression in VSMC [2].
• The RAS exerts its effects by the generation of a family of bioactive angiotensin peptides in which angiotensin II (ANG II) and the angiotensin type 1 (AT1) and angiotensin type 2 (AT2) receptors are most well characterised [25].
• Here we have used computational docking as a guide for the identification of available NSC-65828 and C-181431 analogues that bind more tightly to ANG, and for the characterization of inhibitor binding modes [26].
• Application of losartan intracerebroventricularly (i.c.v.) at 0.5 mg/kg suppressed central ANG II-stimulated plasma AVP release [27].
• Central ANG II induced fetal plasma vasopressin increase was not altered by PD123319 [27].

Physical interactions of ANG

• The augmented intrarenal ANG II coupled with sustained levels of AT1 receptors contribute to the continued ANG II dependent suppression of renal function and sodium excretion thereby maintaining the hypertension [28].
• ANG II had no effect on the binding of EGF to the high-affinity receptor from 1 to 20 h and did not alter receptor downregulation [29].

Enzymatic interactions of ANG

• ANG II increased (P < 0.05) phosphorylated ERK1/2 protein levels [30].

Regulatory relationships of ANG

• Furthermore, ANG II treatment significantly induced VEGF mRNA and protein expression only in VSMC cultured in HG and not NG [2].
• The current studies were undertaken to verify whether vascular response to ANG II is increased in adult offspring of low-protein fed dams (LP) compared with control (CTRL) and if so, to examine underlying mechanism(s) [31].
• Tumor necrosis factor reduced ANG II- and potassium-induced aldosterone synthesis and CYP11B2 mRNA levels [32].
• ANG II induces secretion and activation of transforming growth factor-beta (TGF-beta) by glomerular mesangial cells [33].
• Furthermore, ANG II-induced TSP-1 production is dependent on p38 MAPK and JNK signaling [33].

Other interactions of ANG

• Hypoxic conditions stimulated the secretion of ANG (2.5-fold vs normoxia, P<0.001) and VEGF (3.2-fold vs normoxia, P<0.001) by PTEC [34].
• The presence of ANG, VEGF and hypoxia-inducible factor-1 (HIF-1) was studied by immunofluorescence techniques [34].
• The messenger RNAs (mRNAs) of ANG and VEGF in the PTEC were examined by real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR) [34].
• The K(i) value for RNase A is increased by a factor of >10(8), from 36 fM to >4 microM, and the selectivity factor for ANG is now >10(9) [35].
• The K(i) value for ANG with the deletion variant is 1.1 fM, only 2-fold higher than with WT RI [35].

Analytical, diagnostic and therapeutic context of ANG

• The levels of angiogenin (ANG) and vascular endothelial growth factor (VEGF) in the cell supernatants were measured by enzyme-linked immunosorbent assay [34].
• Reverse transcription-polymerase chain reaction and immunoassay confirmed that LNCaP-CR cells expressed high levels of ANG but not vascular endothelial growth factor (VEGF), compared with the parental LNCaP cells [3].
• The cDNA microarray analysis and protein array of secreted factors indicated angiogenin (ANG), an angiogenic factor, as a candidate gene [3].
• This variant may have potential utility both as an anticancer drug targeting ANG and as a tool for the investigation of the biological function of ANG [35].
• Exaggerated vasomotor response to ANG II in rats with fetal programming of hypertension associated with exposure to a low-protein diet during gestation [31].

References