The Polyamine Pathway as a Potential Target for Vascular Diseases: Focus on Restenosis

Forte, Amalia; Hellstrand, Per; Nilsson, Bengt‐Olof; Grossi, Mario; Rossi, Francesco; Cipollaro, Marilena

doi:10.2174/157016111797484116

Cited by 7 publications

(7 citation statements)

References 87 publications

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“…Considering the multiplicity of phenomena in which polyamines are involved, they could play a key role in restenosis progression, as well as to show a potential as therapeutic targets to prevent or reduce this recurrent pathophysiological phenomenon. Indirect evidence for a role of polyamines in stenosis progression has come from preclinical models of vascular injury [5][6][7][8]. These findings further supported a role for growth-and migration-stimulatory polyamines in stenosis progression.…”

Section: Introductionmentioning

confidence: 81%

Local inhibition of ornithine decarboxylase reduces vascular stenosis in a murine model of carotid injury

Forte

Grossi

Turczyńska

et al. 2013

International Journal of Cardiology

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Section: Introductionmentioning

confidence: 81%

Local inhibition of ornithine decarboxylase reduces vascular stenosis in a murine model of carotid injury

Forte

Grossi

Turczyńska

et al. 2013

International Journal of Cardiology

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“…As arginase competes with NOS for L-arginine, changes in arginase activity can affect NO bioavailability. Moreover, L-ornithine is the principal precursor for production of polyamines required for cell proliferation and differentiation, which is a main feature of atherosclerotic lesions and restenosis (Forte et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Major depression induces oxidative stress and platelet hyperaggregability

Carmo¹,

Mendes-Ribeiro

Matsuura³

et al. 2015

Journal of Psychiatric Research

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“…Arginase converts L-arginine to urea and L-ornithine, precursor amino acids for polyamines involved in smooth muscle cell (SMC) proliferation and dedifferentiation. [36][37][38][39] Incubation of HAoSMCs with erythrocyte membranes from apoE −/− RBC.ARG1-knockout mice significantly increased mRNA levels of ornithine to the total atherosclerotic plaque area on the same section. Findings in male and female mice were compared using Mann-Whitney test, the results are shown within the graph.…”

Section: Altered Vascular Smooth Muscle Cell L-arginine Metabolism An...mentioning

confidence: 97%

Arginase-1 Deletion in Erythrocytes Promotes Vascular Calcification via Enhanced GSNOR (S-Nitrosoglutathione Reductase) Expression and NO Signaling in Smooth Muscle Cells

Gogiraju

Renner

Bochenek

et al. 2022

ATVB

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BACKGROUND: Erythrocytes (red blood cells) participate in the control of vascular NO bioavailability. The purpose of this study was to determine whether and how genetic deletion of ARG1 (arginase-1) affects vascular smooth muscle cell NO signaling, osteoblastic differentiation, and atherosclerotic lesion calcification. METHODS: Atherosclerosis-prone mice with conditional, erythrocyte-restricted deletion of ARG1 (apoE −/− red blood cell.ARG1 knockout) were generated and vascular calcification studied using molecular imaging of the osteogenic activity agent OsteoSense, Alizarin staining or immunohistochemistry, qPCR of osteogenic markers and ex vivo assays. RESULTS: Atherosclerotic lesion size at the aortic root did not differ, but calcification was significantly more pronounced in apoE −/− mice lacking erythrocyte ARG1. Incubation of murine and human VSMCs with lysed erythrocyte membranes from apoE −/− red blood cell. ARG1-knockout mice accelerated their osteogenic differentiation, and mRNA transcripts of osteogenic markers decreased following NO scavenging. In addition to NO signaling via sGC (soluble guanylyl cyclase), overexpression of GSNOR (S-nitrosoglutathione reductase) enhanced degradation of S-nitrosoglutathione to glutathione and reduced protein S-nitrosation of HSP (heat shock protein)-70 were identified as potential mechanisms of vascular smooth muscle cell calcification in mice lacking ARG1 in erythrocytes, and calcium phosphate deposition was enhanced by heat shock and prevented by GSNOR inhibition. Messenger RNA levels of enzymes metabolizing the arginase products L-ornithine and L-proline also were elevated in VSMCs, paralleled by increased proliferation, myofibroblast marker and collagen type 1 expression. CONCLUSIONS: Our findings support an important role of erythrocyte ARG1 for NO bioavailability and L-arginine metabolism in VSMCs, which controls atherosclerotic lesion composition and calcification.

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The Polyamine Pathway as a Potential Target for Vascular Diseases: Focus on Restenosis

Cited by 7 publications

References 87 publications

Local inhibition of ornithine decarboxylase reduces vascular stenosis in a murine model of carotid injury

Local inhibition of ornithine decarboxylase reduces vascular stenosis in a murine model of carotid injury

Major depression induces oxidative stress and platelet hyperaggregability

Arginase-1 Deletion in Erythrocytes Promotes Vascular Calcification via Enhanced GSNOR (S-Nitrosoglutathione Reductase) Expression and NO Signaling in Smooth Muscle Cells

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