Murine Macrophages Produce Endothelin-1 After Microbial Stimulation

Wahl, Jeffrey R.; Goetsch, Nicholas J.; Young, Heather; Maanen, Ryan J. Van; Johnson, Jason D.; Pea, A. S.; Brittingham, Andrew

doi:10.1177/153537020523000907

Cited by 36 publications

(23 citation statements)

References 27 publications

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“…Besides basal vasoconstriction, they are known to exert mitogenic and anti-apoptotic actions [82,83] , as well as act as growth-promoting factors involved in embryonic and fetal development [84][85][86] . It has been reported that macrophages and monocytes act as a source of ET-1 production during infection and inflammation [87,88] . We have recently reported the expression of ET, especially ET-1 in AMC [89] .…”

Section: Nature Of Amcmentioning

confidence: 99%

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

Kaur

Dheen

Ling

2007

Acta Pharmacologica Sinica

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Amoeboid microglial cells (AMC) in the developing brain are active macrophages. The macrophagic nature of these cells has been demonstrated by many methods, such as the localization of various hydrolytic enzymes and the presence of complement type 3 surface receptors in them. More importantly is the direct visualization of these cells engaged in the phagocytosis of degenerating cells at the ultrastructural level. Further evidence of them being active macrophages is the avid internalization of tracers administered by the intravenous or intraperitoneal routes in developing rats. The potential involvement of AMC in immune functions is supported by the induced expression of major histocompatibility complex class I and II antigens on them when challenged by lipopolysaccharide or interferon-γ. Immunosuppressive drugs, such as glucocorticoids and immune function-enhancing drugs like melatonin, affect the expression of surface receptors and antigens and the release of cytokines by AMC. Recent studies in our laboratory have shown the expression of insulin-like growth factors, endothelins, 2',3'-cyclic nucleotide 3'-phosphodiesterase, and N-methyl-D-asparate receptors. This along with the release of chemokines, such as stromal derived factor-1a and monocyte chemoattractant protein-1, suggests multiple functional roles of AMC in early brain development.

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Section: Nature Of Amcmentioning

confidence: 99%

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

Kaur

Dheen

Ling

2007

Acta Pharmacologica Sinica

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“…Alternative cleavage of big ET-1 by matrix metalloproteinase or chymase leads to production of extended-length isoforms, ET-1 and ET-1 , respectively (33,107). Although endothelial cells are considered the primary physiological source of vascular ET-1, it is now recognized that the vascular smooth muscle cells (VSMC), fibroblasts, and inflammatory cells (such as macrophages and leukocytes) are capable of ET-1 production under pathological conditions (28,45,50,52,88,101).…”

Section: Endothelin: Backgroundmentioning

confidence: 99%

Endothelin in the female vasculature: a role in aging?

Lekontseva

Chakrabarti

Davidge

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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vascular diseases are the leading cause of morbidity and mortality in the world. Aging is associated with an increased incidence of cardiovascular disease. Premenopausal women are relatively protected from vascular alterations compared with age-matched men, likely due to higher levels of the female sex hormones. However, these vasoprotective effects in women are attenuated after menopause. Thus, the vascular system in aging women is affected by both the aging process as well as loss of hormonal protection, positioning women of this age group at a high risk for cardiovascular diseases such as hypertension, myocardial infarction, and stroke. The endothelin system in general and endothelin-1 (ET-1) in particular plays an important role in the pathogenesis of vascular dysfunction associated with aging. Evidence suggests that the female sex steroids can interfere with the vascular expression and actions of ET-1 via several mechanisms, which may further contribute to pathological processes in the vasculature of aging women. In this review, we have summarized hormone-dependent vascular pathways whereby ET-1 may mediate the deleterious effects of aging in postmenopausal females.ET-1; menopause; estrogen; vasoconstriction; inflammation AGING OF THE VASCULAR SYSTEM is a complex process characterized by sustained proinflammatory and proconstrictor changes in the vascular microenvironment. The resulting structural and functional alterations in systemic vasculature lead to increased risk of cardiovascular diseases such as hypertension, myocardial infarction, and stroke in the aging population (12,18,51,70). In the absence of chronic preexisting conditions, such as diabetes, premenopausal women express a favorable cardiovascular phenotype compared with age-matched men, largely due to the vasoprotective role of ovarian steroids such as estrogen (92). An alteration in circulating sex hormones at menopause, such as the decrease in estrogens and a relative excess of androgens, is associated with the conversion from a low-to high-risk cardiovascular profile (19,56). Although the mechanisms underlying the pathogenesis of vascular dysfunction in postmenopausal women are not completely understood, it is believed to result from a complex interplay between the aging process and the decline in ovarian hormones like estrogen.Endothelin has emerged as one of the key mediators of vascular dysfunction and remodeling in aging. Interestingly, there is evidence that female sex steroids (in particular, estrogen) can regulate the endothelin system at various levels from gene transcription and posttranslational modification of the peptide to expression of its vascular receptors and postreceptor signaling events. This review will summarize current knowledge on the impact of aging and female sex hormones on the endothelin system, as well as outline directions where further research is needed. A better understanding of the role of endothelin in the pathogenesis of vascular dysfunction in postmenopausal women may lead to the development of novel sex-...

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“…TNF-α can provoke release of ET-1 from macrophages (11,12), and has been observed in combination with ET-1 to promote constriction in the coronary microvascular bed (44). During mental stress in patients with CAD, disinhibition of macrophages consequent to withdrawal of vagal efferent activity may thereby accelerate the production and release of ET-1 from macrophages and/or adjacent endothelial cells that secrete the peptide (17,45). Furthermore, Ach may affect the synthesis and release of ET-1 through action on endothelial cells, since it is known to stimulate the synthesis of NO and, in turn, NO inhibits the synthesis and release of ET-1 (46,47).…”

Section: A N G E R P a R A S Y M P A T H E T I C W I T H D R A W A mentioning

confidence: 99%

Autonomic Contribution to Endothelin-1 Increase during Laboratory Anger-Recall Stress in Patients with Coronary Artery Disease

Burg

Soufer

Lampert

et al. 2011

Mol Med

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In coronary artery disease (CAD), endothelin-1 (ET-1) is released by activated macrophages and thereby contributes to coronary plaque rupture and triggered cardiac events. The multifactorial regulation of ET-1 includes stimulated release by cytokines and autonomic factors. Laboratory stress provokes alteration in autonomic tone and prolonged ET-1 mediated endothelial dysfunction. The objective of the study is to determine the autonomic contribution to an increase in ET-1 in response to laboratory stress in patients with CAD. Patients (n = 88) with chronic stable CAD instrumented with hemodynamic monitor, digital electrocardiogram (ECG) monitor and indwelling catheter for blood sampling completed a laboratory protocol that included initial rest (30 min), baseline (BL: 10 min), and anger recall stress (AR: 8 min). Change from BL to AR was determined for (a) parasympathetic activity (by spectral analysis of ECG); (b) sympathetic activity (by circulating catecholamines); and (c) ET-1. AR provoked increases from BL in catecholamines, and a decrease in parasympathetic activity. Multivariate analysis with change in parasympathetic activity and catecholamines, while controlling for age and use of β-blockers, revealed a significant odds ratio (OR = 3.27, 95% CI 1.03, 10.41 P = 0.04) for an increase in ET-1 associated with parasympathetic withdrawal; no other variables were significant. The predominant influence of parasympathetic activity on anger/stress-provoked increase in ET-1 is consistent with the cholinergic antiinflammatory pathway. Future examination of autonomic influences on atherosclerotic leukocytes, endothelial cell function and the dynamics of ET-1 are warranted.

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Murine Macrophages Produce Endothelin-1 After Microbial Stimulation

Cited by 36 publications

References 27 publications

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

Endothelin in the female vasculature: a role in aging?

Autonomic Contribution to Endothelin-1 Increase during Laboratory Anger-Recall Stress in Patients with Coronary Artery Disease

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