Phenylethanolamine N-Methyl Transferase Expression in Mouse Thymus and Spleen

Warthan, Michelle D; Freeman, Jessica G.; Loesser, Kathryn E.; Lewis, Carolene W.; Hong, Min Hee; Conway, Carolyn M.; Stewart, Jesse C.

doi:10.1006/brbi.2001.0637

Cited by 25 publications

(10 citation statements)

References 16 publications

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“…Extra-adrenal sources of the EPI-synthesizing enzyme, phenylethanolamine N-methytransferase (PNMT) and measurable tissue levels of EPI have been reported by several laboratories, but these tissues do not appear to contribute in a significant manner to circulating EPI levels in laboratory rats. For example, EPI has been quantified in cardiac tissue (Caramona & Soares da Silva, 1985) and PNMT mRNA levels have been detected in several tissues, including skin (Pullar et al, 2006), spleen (Andreassi et al, 1998;Warthan et al, 2002), thymus (Andreassi et al, 1998;Warthan et al, 2002), cardiac tissue (Goncalvesova et al, 2004;Krizanova et al, 2001;Kvetnansky et al, 2006) and sympathetic ganglia Kvetnansky et al, 2006).…”

Section: Stressmentioning

confidence: 99%

Learning about stress: neural, endocrine and behavioral adaptations

McCarty

2016

Stress

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In this review, nonassociative learning is advanced as an organizing principle to draw together findings from both sympathetic-adrenal medullary and hypothalamic-pituitary-adrenocortical (HPA) axis responses to chronic intermittent exposure to a variety of stressors. Studies of habituation, facilitation and sensitization of stress effector systems are reviewed and linked to an animal's prior experience with a given stressor, the intensity of the stressor and the appraisal by the animal of its ability to mobilize physiological systems to adapt to the stressor. Brain pathways that regulate physiological and behavioral responses to stress are discussed, especially in light of their regulation of nonassociative processes in chronic intermittent stress. These findings may have special relevance to various psychiatric diseases, including depression and post-traumatic stress disorder (PTSD).

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Section: Stressmentioning

confidence: 99%

Learning about stress: neural, endocrine and behavioral adaptations

McCarty

2016

Stress

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“…Interestingly, PNMT levels were found to be two-fold higher in the lymphocyte-harboring cortex of the thymus than in the medulla. Low PNMT activity and PNMT mRNA also could be detected in the marginal zone of the white pulp of the spleen (20), which contains significant amounts of lymphocytes also, suggesting the presence of epinephrinegenerating cell population(s) in lymphoid organs. As the morphology of these findings correlate perfectly with the lymphocyte-rich sites of lymphoid organs, it is reasonable to assume that the epinephrine-producing cell population might be lymphocytes.…”

Section: Immune Cells-a New Diffusely Expressed Adrenergic Organmentioning

confidence: 99%

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

166

114

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It is well established that catecholamines (CAs), which regulate immune and inflammatory responses, derive from the adrenal medulla and from presynaptic neurons. Recent studies reveal that T cells also can synthesize and release catecholamines which then can regulate T cell function. We have shown recently that macrophages and neutrophils, when stimulated, can generate and release catecholamines de novo which, then, in an autocrine/paracrine manner, regulate mediator release from these phagocytes via engagement of adrenergic receptors. Moreover, regulation of catecholamine-generating enzymes as well as degrading enzymes clearly alter the inflammatory response of phagocytes, such as the release of proinflammatory mediators. Accordingly, it appears that phagocytic cells and lymphocytes may represent a major, newly recognized source of catecholamines that regulate inflammatory responses.

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“…For example, adrenaline (A) and NA produced by sympathetic nerves may modulate cellular function by acting on β-2 adrenergic receptors of B and Th1 cells [6]. In addition, catecholamine biosynthetic enzymes are expressed in the lymphoid organs [7], as well as in neutrophils and macrophages [8]. It is known that normal catecholaminergic turnover results from balance among synthesis, release, and reuptake of catecholamines.…”

Section: Introductionmentioning

confidence: 99%

Animal Models for Chronic Stress-Induced Oxidative Stress in the Spleen: The Role of Exercise and Catecholaminergic System

Gavrilović¹,

Stojiljković²,

Popović³

et al. 2018

Experimental Animal Models of Human Diseases - An Effective Therapeutic Strategy

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We examined the effects of daily exercise on the gene expression of catecholamine biosynthetic enzymes (tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), and phenyl ethanolamine N-methyltransferase (PNMT)), vesicular monoamine transporter 2 (VMAT 2), antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)), concentrations of catecholamines (noradrenaline (NA) and adrenaline (A)) and malondialdehyde (MDA), activities of monoamine oxidase (MAO), and antioxidant enzymes in the spleen of chronically psychosocially stressed rats. Exposure of chronically stressed rats to exercise increased the levels of PNMT protein by 19%, VMAT 2 mRNA by 100%, NA by 160%, and A by 140%; decreased/unchanged MAO enzyme activity; returned concentrations of MDA to control level; and increased CAT and GPx mRNA levels (50% and 150%, respectively). Exercise induced the accumulation of the catecholamines and a decrease of stress-induced oxidative stress in the spleen, which may significantly affect the immune-neuroendocrine interactions in stress conditions. Also, exercise induced the catecholaminergic system and antioxidant defense to become more ready to a novel stressor, which indicates that exercise may induce potentially positive physiological adaptations. Our combined model of chronic social isolation and long-term daily treadmill running in rats may be a good animal model in the research of therapeutic role of exercise in human disease caused by chronic stress.

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Phenylethanolamine N-Methyl Transferase Expression in Mouse Thymus and Spleen

Cited by 25 publications

References 16 publications

Learning about stress: neural, endocrine and behavioral adaptations

Learning about stress: neural, endocrine and behavioral adaptations

Catecholamines—Crafty Weapons in the Inflammatory Arsenal of Immune/Inflammatory Cells or Opening Pandora’s Box?

Animal Models for Chronic Stress-Induced Oxidative Stress in the Spleen: The Role of Exercise and Catecholaminergic System

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