Nitric oxide synthase modulates angiogenesis in response to tissue ischemia.

Murohara, Toyoaki; Asahara, Takayuki; Silver, Marcy; Bauters, Christophe; Masuda, Haruchika; Kalka, Christoph; Kearney, Marianne; Chen, D; Symes, James F.; Fishman, Mark C.; Huang, Paul L.; Isner, Jeffrey M.

doi:10.1172/jci1560

Cited by 1,125 publications

(967 citation statements)

References 51 publications

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“…26 Inhibitors of eNOS decrease VEGF-induced angiogenesis. 27,28 In addition, ischemia-induced angiogenesis is reduced in eNOS knockout mice, 29 and in rat models, oral folate can rescue this process in a NO-dependent manner. 30 eNOS production of NO depends on the cofactor BH 4 .…”

Section: Psma Expression In Tumor Neovasculaturementioning

confidence: 99%

Prostate-specific membrane antigen expression in regeneration and repair

et al. 2008

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Prostate-specific membrane antigen is a type II transmembrane glycoprotein, expressed in benign and neoplastic prostatic tissue as well as endothelial cells of neovasculature from a variety of tumors. The expression of prostate-specific membrane antigen in nonneoplastic neovasculature has not been well studied. Therefore, we studied nonneoplastic reparative and regenerative human tissues, as well as preneoplastic tissue, to determine the presence of prostate-specific membrane antigen-expressing neovasculature. Formalinfixed paraffin-embedded tissue from keloids, granulation tissue from heart valves and pleura, proliferative and secretory endometrium, and Barrett's mucosa with and without dysplasia were stained for the expression of prostate-specific membrane antigen (3E6). Vessels of proliferative, mid-secretory, and late secretory endometrium were consistently strongly positive for prostate-specific membrane antigen expression in all ten cases of each type (100%). Vessels associated with granulation tissue from pleural peels and heart valves were positive in 10 of 12 cases (83%) and 7 of 10 cases (70%), respectively. Keloids had prostate-specific membrane antigen-expressing endothelial cells in 6 of 15 cases (40%). Prostate-specific membrane antigen was not expressed by vessels associated with Barrett's mucosa with low-grade dysplasia (12 foci), high-grade dysplasia (24 foci), or no dysplasia (18 foci). A variety of nonneoplastic neovasculature expresses prostatespecific membrane antigen, including vessels in proliferative endometrium, granulation tissue, and some scars. This is the first study showing that prostate-specific membrane antigen is expressed in neovasculature from physiologic regenerative and reparative conditions. The folate hydrolase activity of prostate-specific membrane antigen may facilitate vasculogenesis and angiogenesis by increasing local availability of folic acid. These findings will enhance our overall understanding of blood vessel development and will enable us to better understand the effects of anti-prostate-specific membrane antigen therapies, which are already being explored in clinical trials.

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Section: Psma Expression In Tumor Neovasculaturementioning

confidence: 99%

Prostate-specific membrane antigen expression in regeneration and repair

et al. 2008

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“…48,49 As it was clearly demonstrated that laser Doppler flow velocity correlates well with the capillary density, 48,49 we measured the cardiac blood flow by means of a laser Doppler blood flow meter (Laser Doppler Image, Moor Instruments, Devon, UK). Indeed, we confirmed that the blood flow measured by LDI correlated well with the capillary den-sity (data not shown).…”

Section: Monitoring Cardiac Blood Flowmentioning

confidence: 99%

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets

et al. 2000

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The feasibility of a novel therapeutic strategy using angiogenic growth factors to expedite and/or augment collateral artery development has recently entered the realm of treatment of ischemic diseases. Hepatocyte growth factor (HGF) is a novel member of endothelium-specific growth factors whose mitogenic activity on endothelial cells is very potent. Although it has been demonstrated that HGF is a potential angiogenic growth factor in in vitro culture systems, there is no direct in vivo evidence for the angiogenic activity of HGF in physiological conditions. In this study, we hypothesized that transfection of HGF gene into infarcted myocardium could induce angiogenesis, potentially resulting in a beneficial response to hypoxia. Human HGF gene or control vector driven by the SR␣ promoter was transfected into rat myocardium by the HVJ-liposome method. Four days after in vivo transfection of human HGF gene, there was a marked increase in human immunoreactive HGF as compared with control vector (P Ͻ 0.01). In myocardium transfected with HGF vector, a significant increase in PCNA-positive endothelial cells was observed, while few PCNA-positive endothelial cells were detected in both control-vector-transfected and untreated myocardium. The number of vessels around

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“…NO also modulates vascular permeability [6][7][8], angiogenesis [9,10], platelet adhesion and aggregation [11][12][13], and leukocyte adhesion [14][15][16]. Thus, NO bioavailabilty is important in maintaining several aspects of homeostasis and its dysfunction contributes to a large variety of diseased states [17][18][19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

The potential of Angeli's salt to decrease nitric oxide scavenging by plasma hemoglobin

Azarov

Jeffers

et al. 2008

Free Radical Biology and Medicine

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Release of hemoglobin from the erythrocyte during intravascular hemolysis contributes to the pathology of a variety of diseased states. This effect is partially due to the enhanced ability of cellfree plasma hemoglobin, which is primarily found in the ferrous, oxygenated state, to scavenge nitric oxide. Oxidation of the cell-free hemoglobin to methemoglobin, which does not effectively scavenge nitric oxide, using inhaled nitric oxide has been shown to be effective in limiting pulmonary and systemic vasoconstriction. However, the ferric heme species may be reduced back to ferrous hemoglobin in plasma and has the potential to drive injurious redox chemistry. We propose that compounds that selectively convert cell-free hemoglobin to ferric, and ideally iron-nitrosylated heme species that do not actively scavenge nitric oxide would effectively treat intravascular hemolysis. We show here that nitroxyl, generated by Angeli's salt (Sodium α-oxyhyponitrite, Na 2 N 2 O 3 ), preferentially reacts with cell-free hemoglobin compared to that encapsulated in the red blood cell under physiologically relevant conditions. Nitroxyl oxidizes oxygenated ferrous hemoglobin to methemoglobin and can convert the methemoglobin to a more stable, less toxic species, iron-nitrosyl hemoglobin. These results support the notion that Angeli's salt or a similar compound could be used to effectively treat conditions associated with intravascular hemolysis.

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Nitric oxide synthase modulates angiogenesis in response to tissue ischemia.

Cited by 1,125 publications

References 51 publications

Prostate-specific membrane antigen expression in regeneration and repair

Prostate-specific membrane antigen expression in regeneration and repair

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets

The potential of Angeli's salt to decrease nitric oxide scavenging by plasma hemoglobin

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