Endothelin-1 decreases ethanolamine plasmalogen levels and evokes PAF production in brain microvessels

Collado, M. Pilar; Latorre, Eduardo; Fernández, Inmaculada; Aragonés, M.D.; Catalán, Rosa

doi:10.1016/j.mvr.2003.08.002

Cited by 6 publications

(3 citation statements)

References 30 publications

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“…This study showed that 2-AG counteracts calcium mobilization and cytoskeleton rearrangements induced by ET-1 suggesting that the crosstalk between these two neurotransmitter systems might be relevant for the regulation of cerebral capillary and microvascular function. In addition, treatment of brain microvessels with ET-1 decreases sphyngomyelin and ethanolamine plasmalogen levels, increases ceramides levels and evokes platelet activating factor (PAF) production via ET A receptors [22,23]. In human brain-derived endothelial cells, ET-1 induces interleukin-8 production via the stimulation of ET A receptors and by signalling pathways involving the activation of protein kinases and protein tyrosine kinases [193].…”

Section: Endotheliummentioning

confidence: 99%

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Schinelli¹

2006

CMC

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The endothelin system, consisting of three peptides, two peptidases and two G-protein coupled receptors, is widely expressed in the brain cell types and brain-derived tumor cell lines. The stimulation of endothelin receptors elicits a variety of short- and long-term changes at cellular level but the effects of the pharmacological modulation of the endothelin system in brain physiology and pathophysiology are, at the present time, poorly understood. Altered expression of endothelins (ETs) in reactive astrocytes has been observed in many pathological conditions of the human brain, such as infarcts, lacunae, traumatic conditions, Alzheimer's disease and inflammatory diseases of the brain. In addition, recent studies have shown that endothelin antagonists might inhibit growth and induce cell death in human melanoma cells in vitro and in vivo, and have emphasized a possible role of endothelin peptides as autocrine or paracrine factor in the proliferation and dissemination of tumor cell lines. Given the fact that brain cell and a variety of brain tumor cell lines express functional endothelin receptors, further studies are warranted to demonstrate a possible therapeutic role of endothelin agonists and antagonist in the pharmacological treatment of brain-related diseases and brain tumors.

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Section: Endotheliummentioning

confidence: 99%

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Schinelli¹

2006

CMC

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“…Endothelin-1 has been shown to increase the production of PAF in a variety of cells and tissues. [9][10][11][12][13][14][15] Conversely, PAF has been shown to activate ET-1 receptors. 16 These mediators have been shown to act synergistically to decrease perfusion and increase inflammation in several animal models, including bacteremia-induced lung injury, 17 acute pancreatitis, 18 posttransplant lung ischemia/reperfusion, 19 small intestine microcirculation, 20 and peritonitis.…”

Section: Introductionmentioning

confidence: 99%

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

et al. 2012

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The significance of endothelin-1 (ET-1) in platelet-activating factor (PAF)-induced fetal growth restriction (FGR) was evaluated in timed-pregnant rats receiving intravenous carbamyl-PAF (c-PAF; 0.5, 1.0, or 2.5 µg/kg per h) or vehicle, with or without ET-1 receptor A (ET(A)) antagonist (10 or 20 mg/kg per d) for 7 days beginning on gestation day 14. Tissues were collected on day 21. Carbamyl-PAF reduced fetal weights dose dependently. Placental weights were significantly reduced but not dose dependently. ET(A) antagonism prevented FGR at the 0.5, but not the 1.0 and 2.5 µg/kg per h c-PAF doses. Correspondingly, placental, but not uterine, preproET-1 messenger RNA (mRNA) expression (determined by reverse transcription-polymerase chain reaction) was increased at 0.5 µg/kg per h but not at higher c-PAF doses. In summary, c-PAF infusion results in fetal and placental growth restriction in the rat. At low doses of c-PAF, ET-1 is central to the pathophysiology of PAF-induced FGR. At higher c-PAF doses, FGR is induced by mechanisms other than ET-1 action.

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“…Endothelin 1 (ET1) dysfunction generates superoxide by activation of ETA and ETB receptors, the process is further initiated by the formation of peroxynitrite that downregulates the formation of nitric oxide, and hence, the inflammatory process and oxidative stress are initiated leading to vascular endothelial dysfunction. Preclinical studies have proven that when endothelin receptors are antagonized using drugs such as bosentan they decrease inflammatory mediators and vascular dysfunction in brain carotid arteries hence maintaining cerebrospinal blood flow and are efficient in Alzheimer's with vascular dementia [ 48 ]. Drugs that are used in the improving vasospasm and decreased blood flow target ETA receptors in the brain [ 49 ].…”

Section: Role Of Endothelin Receptors In Alzheimer Diseasementioning

confidence: 99%

Targeting Endothelin in Alzheimer’s Disease: A Promising Therapeutic Approach

Sharma

Behl

Kumar

et al. 2021

BioMed Research International

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Endothelin is a chemical mediator that helps in maintaining balance within the blood-brain barrier by regulating the levels of toxicants and molecules which pass through the brain, suggesting that a rise in its production determines Alzheimer’s disease. The inequity in the amyloid β occurs due to a problem in its clearance from the brain initiating the production of reactive oxygen species and superoxide that activates a cascade wherein the release of inflammatory mediators and various enzymes like endothelin-converting enzymes take place. Furthermore, the cascade increases the levels of endothelin in the brain from endothelial cells. Endothelin levels are upregulated, which can be regulated by modulating the action of endothelin-converting enzymes and endothelin receptors. Hence, endothelin paves a pathway in the treatment of Alzheimer’s disease. In this article, we have covered various mechanisms and preclinical studies that support and direct endothelin involvement in the progression of Alzheimer’s disease by using various search tools such as PubMed, Science Direct, and Medline. Conclusive outcome data were extracted that all together defy contrivance pathways, potential drugs, endothelin receptors, and endothelin enzymes in our article giving profound importance to target endothelin for prevention and treatment of Alzheimer’s disease.

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Endothelin-1 decreases ethanolamine plasmalogen levels and evokes PAF production in brain microvessels

Cited by 6 publications

References 30 publications

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

Targeting Endothelin in Alzheimer’s Disease: A Promising Therapeutic Approach

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