Plasma endothelin-1 immunoreactivity in asthmatic children

El-Gamal, Yehia; Hossny, Elham; Awwad, Khaled S.; Mabrouk, Randa Reda; Boseila, Nahed

doi:10.1016/s1081-1206(10)62366-6

Cited by 8 publications

(5 citation statements)

References 20 publications

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“…Interestingly, previous studies have shown that plasma ET levels were increased in children with VVS ( 29 ), suggesting an imbalance of vascular tone regulators in children with NMS. Similar to the findings in NMS children, plasma ET-1 levels in children with AS significantly increase in the acute attack stage compared with the remission stage ( 30 ). ET-1 is also elevated in the airway epithelium and involved in bronchoconstriction and airway remodeling in patients with AS ( 31 , 32 ), indicating that ET may be a candidate factor related to the pathogenesis of the comorbidity of NMS and AS in children.…”

Section: Pediatric Vvs And/or Pots Comorbid With Allergic Diseasessupporting

confidence: 80%

Comorbidity of Neurally Mediated Syncope and Allergic Disease in Children

Wang

Jin

et al. 2020

Front. Immunol.

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Neurally mediated syncope (NMS) is the most common underlying disease of pediatric syncope, which generally includes vasovagal syncope (VVS), postural tachycardia syndrome (POTS), and situational syncope. Allergic diseases involving the respiratory system, digestive system, skin, and other systems are prevalent in children. In recent years, increasing attention has been paid to children with the comorbidity of NMS and allergic diseases. This article reviews the featured clinical manifestations and pathogenesis of the comorbidity according to the progress of related studies. Clinical studies have shown that the comorbidity rate of pediatric VVS and/or POTS with allergic diseases amounts to ~30–40%, referring to the whole population of children with VVS and/or POTS. Additionally, children with the comorbidity present some relatively special clinical characteristics. A series of mechanisms or regulatory factors relating to allergies, such as the imbalance of vasoactive elements, dysfunction of the autonomic nervous system (ANS), and autoimmunity may play a role in the development of the comorbidity. Moreover, 90% of children with cough syncope, a type of situational syncope, have a history of asthma, indicating a potential relationship between asthma and NMS. Further studies exploring the clinical characteristics and pathogenesis of the comorbidity are still needed to aid in the diagnosis and treatment of children with NMS.

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Section: Pediatric Vvs And/or Pots Comorbid With Allergic Diseasessupporting

confidence: 80%

Comorbidity of Neurally Mediated Syncope and Allergic Disease in Children

Wang

Jin

et al. 2020

Front. Immunol.

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“…Therefore, we cannot discard the possibility that other mechanisms besides Ca 2ϩ mediate the CH-induced activation of calcineurin/NFAT. In addition, other humoral factors that are upregulated by hypoxia could contribute to the increased NFAT activity demonstrated in this study, such as ET-1 and Ang II (4,36,37,(63)(64)(65)(66)(67)(68)(69)(70).…”

Section: Ch Induces Nfatc3 Activation In Pulmonarymentioning

confidence: 80%

NFATc3 Mediates Chronic Hypoxia-induced Pulmonary Arterial Remodeling with α-Actin Up-regulation

Garcı́a

Spangler

Alò

et al. 2007

Journal of Biological Chemistry

100

130

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Physiological responses to chronic hypoxia include polycythemia, pulmonary arterial remodeling, and vasoconstriction. Chronic hypoxia causes pulmonary arterial hypertension leading to right ventricular hypertrophy and heart failure. During pulmonary hypertension, pulmonary arteries exhibit increased expression of smooth muscle-␣-actin and -myosin heavy chain. NFATc3 (nuclear factor of activated T cells isoform c3), which is a Ca 2؉ -dependent transcription factor, has been recently linked to smooth muscle phenotypic maintenance through the regulation of the expression of ␣-actin. The aim of this study was to determine if: (a) NFATc3 is expressed in murine pulmonary arteries, (b) hypoxia induces NFAT activation, (c) NFATc3 mediates the up-regulation of ␣-actin during chronic hypoxia, and (d) NFATc3 is involved in chronic hypoxia-induced pulmonary vascular remodeling. NFATc3 transcript and protein were found in pulmonary arteries. NFAT-luciferase reporter mice were exposed to normoxia (630 torr) or hypoxia (380 torr) for 2, 7, or 21 days. Exposure to hypoxia elicited a significant increase in luciferase activity and pulmonary arterial smooth muscle nuclear NFATc3 localization, demonstrating NFAT activation. Hypoxia induced up-regulation of ␣-actin and was prevented by the calcineurin/NFAT inhibitor, cyclosporin A (25 mg/kg/day s.c.). In addition, NFATc3 knock-out mice did not showed increased ␣-actin levels and arterial wall thickness after hypoxia. These results strongly suggest that NFATc3 plays a role in the chronic hypoxia-induced vascular changes that underlie pulmonary hypertension.As altitude increases, the barometric pressure and atmospheric oxygen partial pressure decrease. This decrease in barometric pressure is the basic cause of all hypoxia-related problems in high altitude pathophysiology. Similar levels of hypoxia are present in patients with chronic bronchitis, emphysema, cystic fibrosis, asthma, and severe restrictive lung diseases (1). Chronic hypoxia (CH) 2 causes pulmonary hypertension due to pulmonary vasoconstriction, arterial remodeling, and polycythemia, which ultimately results in right ventricular (RV) hypertrophy and often heart failure (2). Pulmonary vasoconstriction is thought to be caused by elevated vascular tone through increased pulmonary arterial smooth muscle cell (PASMC) intracellular Ca 2ϩ ([Ca 2ϩ ] i ) (3-8) and increased sensitivity of the contractile apparatus to Ca 2ϩ (9 -12).Regardless of the cause of pulmonary hypertension, the structural change that is thought to underlie the increased vascular resistance is remodeling of small pulmonary arteries. A prominent feature of this vascular remodeling is medial thickening. In proximal pulmonary vessels, medial enlargement is caused by hypertrophy and hyperplasia of the pre-existing smooth muscle cells (reviewed in Ref.

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“…A serum IgE level was considered elevated if it exceeded the highest reference value for age (18). The value used in correlation analysis was the percentage from the highest normal value for age (patient’s actual value/ highest normal value for age multiplied by 100) (19). Subjects in the control group with elevated serum total IgE levels were excluded from the study.…”

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confidence: 99%

Vascular endothelial growth factor overexpression in induced sputum of children with bronchial asthma

Hossny¹,

El-Awady²,

Bakr

et al. 2009

Pediatric Allergy Immunology

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Vascular endothelial growth factor (VEGF) induces angiogenesis and increases vascular permeability participating in narrowing of the airway lumen that follows lung injury. We sought to investigate the expression of VEGF in induced sputum during and after recovery from acute episodes of bronchial asthma in children. Eighteen asthmatic children with acute attacks of varying severity were subjected to VEGF estimation by an enzymatic immunoassay in induced sputum. They were followed up till complete remission of symptoms and signs and were then retested. VEGF was also estimated in sputum induced from age 34 and sex‐matched healthy children enrolled as a control group. The sputum VEGF levels during acute asthma [median = 71 ng/ml; mean (s.d.) = 114.6 (121.8) ng/ml] were significantly higher than the levels estimated during remission [median = 50 ng/ml; mean (s.d.) = 45.7 (24.2) ng/ml] and both were higher than the corresponding levels of the control group [median = 36 ng/ml; mean (s.d.) = 31.3 (17.2) ng/ml]. VEGF levels during asthmatic episodes correlated positively to the recovery levels (r = 0.6, p = 0.009). The patients’ VEGF expression did not vary with asthma severity, serum total IgE concentration, peripheral blood eosinophil count, or erythrocyte sedimentation rate of patients. Children on corticosteroids inhalation therapy at enrollment had sputum VEGF levels that were comparable to those on other therapies. The increased expression of sputum VEGF in asthmatic children reinforces the concept that it might have a pathogenetic role in bronchial asthma and may represent a biomarker of airway inflammation.

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Plasma endothelin-1 immunoreactivity in asthmatic children

Cited by 8 publications

References 20 publications

Comorbidity of Neurally Mediated Syncope and Allergic Disease in Children

Comorbidity of Neurally Mediated Syncope and Allergic Disease in Children

NFATc3 Mediates Chronic Hypoxia-induced Pulmonary Arterial Remodeling with α-Actin Up-regulation

Vascular endothelial growth factor overexpression in induced sputum of children with bronchial asthma

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