Arginase inhibition reduces interleukin-1β-stimulated vascular smooth muscle cell proliferation by increasing nitric oxide synthase-dependent nitric oxide production

Yoon, Jeongyeon; Ryoo, Sungwoo

doi:10.1016/j.bbrc.2013.05.002

Cited by 17 publications

(8 citation statements)

References 32 publications

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“…While COX-2 inhibitors have been shown to reduce tumor growth through arginase inhibition (132, 133), administration of diclofenac, a non-steroidal anti-inflammatory drug against COX-2 (134) and phospholipase A 2 (135), was found to cause tumor suppression via a mechanism related to the inhibition of tumor vascularization (136). Although the expression and activity of arginase in the vasculature was not evaluated in this study, it is speculated that the observed tumor suppression is attributable to the inhibition of vascular arginase since this enzyme has been shown to play an important role in the growth of vascular cells (35, 137–139). Although the direct link between COX and arginase in vasomotor regulation remains to be determined, the finding of the close association between these two enzymes in tumor-promoted angiogenesis (140) and in alleviating chronic hypertension and improving vascular endothelial function and vasomotor activity (68) may provide new direction and insights into this underdeveloped research area.…”

Section: Cox and Arginase In Vascular Regulationmentioning

confidence: 98%

Vasomotor Regulation of Coronary Microcirculation by Oxidative Stress: Role of Arginase

Li¹,

Hein²

2013

Front. Immunol.

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Overproduction of reactive oxygen species, i.e., oxidative stress, is associated with the activation of redox signaling pathways linking to inflammatory insults and cardiovascular diseases by impairing endothelial function and consequently blood flow dysregulation due to microvascular dysfunction. This review focuses on the regulation of vasomotor function in the coronary microcirculation by endothelial nitric oxide (NO) during oxidative stress and inflammation related to the activation of L-arginine consuming enzyme arginase. Superoxide produced in the vascular wall compromises vasomotor function by not only scavenging endothelium-derived NO but also inhibiting prostacyclin synthesis due to formation of peroxynitrite. The upregulation of arginase contributes to the deficiency of endothelial NO and microvascular dysfunction in various vascular diseases by initiating or following oxidative stress and inflammation. Hydrogen peroxide, a diffusible and stable oxidizing agent, exerts vasodilator function and plays important roles in the physiological regulation of coronary blood flow. In occlusive coronary ischemia, the release of hydrogen peroxide from the microvasculature helps to restore vasomotor function of coronary collateral microvessels with exercise training. However, excessive production and prolonged exposure of microvessels to hydrogen peroxide impairs NO-mediated endothelial function by reducing L-arginine availability through hydroxyl radical-dependent upregulation of arginase. The redox signaling can be a double-edged sword in the microcirculation, which helps tissue survival in one way by improving vasomotor regulation and elicits oxidative stress and tissue injury in the other way by causing vascular dysfunction. The impact of vascular arginase on the development of vasomotor dysfunction associated with angiotensin II receptor activation, hypertension, ischemia-reperfusion, hypercholesterolemia, and inflammatory insults is discussed.

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Section: Cox and Arginase In Vascular Regulationmentioning

confidence: 98%

Vasomotor Regulation of Coronary Microcirculation by Oxidative Stress: Role of Arginase

Li¹,

Hein²

2013

Front. Immunol.

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“…Differentiated phenotype (contractile phenotype) VSMCs do not proliferate or produce inflammatory mediators [1, 3]. In response to injury, VSMCs change their gene expression profile to a differentiated phenotype (synthetic phenotype or inflammatory phenotype), and begin to produce inflammatory mediators which stimulates VSMC proliferation and migration [46]. On the other hand, some inflammatory mediators ultimately activate transcription factors to initiate gene expression pattern changes associated with VSMC phenotypes to a differentiated phenotype [47].…”

Section: Discussionmentioning

confidence: 99%

NLRP3 Gene Deletion Attenuates Angiotensin II-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells and Vascular Remodeling

Ren

Tong

et al. 2017

Cell Physiol Biochem

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Background/Aims: Angiotensin (Ang) II plays vital roles in vascular inflammation and remodeling in hypertension. Phenotypic transformation of vascular smooth muscle cells (VSMCs) is a major initiating factor for vascular remodeling. The present study was designed to determine the roles of NLRP3 inflammasome activation in Ang II-induced VSMC phenotypic transformation and vascular remodeling in hypertension. Methods: Primary VSMCs from the aorta of NLRP3 knockout (NLRP3^-/-) mice and wild-type (WT) mice were treated with Ang II for 24 h. Subcutaneous infusion of Ang II via osmotic minipump for 2 weeks was used to induce vascular remodeling and hypertension in WT and NLRP3^-/- mice. Results: NLRP3 gene deletion attenuates Ang II-induced NLRP3 inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice VSMCs. Ang II-induced hypertension and vascular remodeling in WT mice were attenuated in NLRP3^-/- mice. Furthermore, Ang II-induced NLRP3 inflammasome activation, phenotypic transformation and proliferating cell nuclear antigen (PCNA) upregulation were inhibited in the media of aorta of NLRP3^-/- mice. Conclusions: NLRP3 inflammasome activation contributes to Ang II-induced VSMC phenotypic transformation and proliferation as well as vascular remodeling and hypertension.

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“…On the other hand, smooth muscle cells of human lung tissue express both isoforms [26,55,59]. In general, ARG expression can be modulated in different sites, depending on the stimulus that is applied [7,41,55,60].…”

Section: Methodsmentioning

confidence: 99%

Untitled

2018

Planta Med

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IntroductionSeveral diseases have been linked to the development of ED, such as atherosclerosis, hypercholesterolaemia, coronary disease, erectile dysfunction, asthma, renal failure, rheumatoid arthritis, periodontitis, psychiatric disorders, and cancer, as well as diseases with a high prevalence, such as diabetes (types 1 and 2) and SAH [1-9].The preservation of the endothelium is fundamental in maintaining the physiology of the vascular system (in the regulation of its tonus, the development of immune, structural, and proliferative functions, and interaction with other cellular types) and also in the prevention of the development/aggravation of diseases [10][11][12].

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Arginase inhibition reduces interleukin-1β-stimulated vascular smooth muscle cell proliferation by increasing nitric oxide synthase-dependent nitric oxide production

Cited by 17 publications

References 32 publications

Vasomotor Regulation of Coronary Microcirculation by Oxidative Stress: Role of Arginase

Vasomotor Regulation of Coronary Microcirculation by Oxidative Stress: Role of Arginase

NLRP3 Gene Deletion Attenuates Angiotensin II-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells and Vascular Remodeling

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