Anti-asthmatic agents alleviate pulmonary edema by upregulating AQP1 and AQP5 expression in the lungs of mice with OVA-induced asthma

Dong, Chunling; Wang, Guifang; Li, Bo; Xiao, Kui; Ma, Zhongsen; Huang, Hua; Wang, Xiangdong; Bai, Chunxue

doi:10.1016/j.resp.2011.12.008

Cited by 57 publications

(53 citation statements)

References 34 publications

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“…The valuable role of glucocorticoids in the conservative treatment of CRS is undeniable; in addition to their anti-inflammatory effects, glucocorticoids can regulate the water balance in multiple tissues (8,25,26). Water transport of the sinonasal mucosa is also noteworthy in the pathogenesis of CRS.…”

Section: Discussionmentioning

confidence: 99%

Effects of glucocorticoid on the expression and regulation of aquaporin 5 in the paranasal sinus of rats with chronic rhinosinusitis

Cui

Lü

et al. 2017

Experimental and Therapeutic Medicine

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Aquaporins (AQPs) are water-specific membrane channel proteins that regulate water homeostasis for cells and organisms. AQP5 serves an important role in the maintenance of mucosal water homeostasis, and potentially contributes to mucosal edema and inflammation formation in chronic rhinosinusitis (CRS). The aim of the present study was to explore the expression pattern of AQP5 and the effect of glucocorticoids on AQP5 expression in rats with CRS. The rats were randomly divided into three equal groups, as follows: CRS, dexamethasone (dexa) treatment and control groups. A polyvinyl acetal material containing Staphylococcus aureus was inserted into the left nasal cavity of each rat from the CRS and dexa groups. On the 90th post-operative day, the dexa group received dexamethasone (2 mg/kg/day) via intraperitoneal injection for 7 days. The controls did not receive any treatment. The expression of AQP5 in the sinonasal mucosa was determined using immunohistochemistry and quantitative PCR. The immunoreactivities of AQP5 were primarily noted in the epithelial lining and glandular cells, the vascular endothelium and in the goblet cells in the sinonasal mucosa. The AQP5 mRNA expression level was significantly higher in the dexa group than in the control and CRS groups (P=0.006 and P=0.014, respectively). However, no significant difference was indicated between the CRS and control groups (P=0.760). In conclusion, the current study suggests that glucocorticoids induce AQP5 expression in the sinonasal mucosa of CRS rats, which highlights AQP5 as a potential target in the diagnosis and treatment of CRS.

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Section: Discussionmentioning

confidence: 99%

Effects of glucocorticoid on the expression and regulation of aquaporin 5 in the paranasal sinus of rats with chronic rhinosinusitis

Cui

Lü

et al. 2017

Experimental and Therapeutic Medicine

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“…AQPs have important roles in the pathogenesis of pulmonary diseases, especially lung cancers. Recently, a mouse model of asthma induced by ovalbumin has been used to study the mRNA and protein expression of AQP1 and AQP5 [12]. The authors found that both AQPs were significantly increased by treatment with dexamethasone, ambroxol, and terbutaline, indicating that AQP1 and AQP5 are closely related to pulmonary edema but not to eosinophil infiltration or mucus secretion in patients with asthma.…”

Section: Discussionmentioning

confidence: 99%

Expression of aquaporins in bronchial tissue and lung parenchyma of patients with chronic obstructive pulmonary disease

Calero

Lόpez-Campos

Izquierdo

et al. 2014

Multidiscip Respir Med

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BackgroundAquaporins AQP1 and AQP5 are highly expressed in the lung. Recent studies have shown that the expression of these proteins may be mechanistically involved in the airway inflammation and in the pathogenesis of chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the expression of AQP1 and AQP5 in the bronchial tissue and the lung parenchyma of patients with COPD and COPD-resistant smokers.MethodsUsing a case–control design, we selected a group of 15 subjects with COPD and 15 resistant smokers (smokers without COPD) as a control, all of whom were undergoing lung resection surgery due to a lung neoplasm. We studied the expression of AQP1 and AQP5 in the bronchial tissue and the lung parenchyma by means of immunohistochemistry and reverse-transcription real-time polymerase chain reaction. Tissue expression of AQP1 and AQP5 was semi-quantitatively assessed in terms of intensity and expression by immunohistochemistry using a 4-point scale ranging from 0 (none) to 3 (maximum).ResultsThere were no significant differences in gene expression between COPD patients and resistant smokers both in the bronchial tissue and in the lung parenchyma. However, AQP1 gene expression was 2.41-fold higher in the parenchyma of smokers with COPD compared to controls, whereas the AQP5 gene showed the opposite pattern, with a 7.75-fold higher expression in the bronchus of smokers with COPD compared with controls. AQP1 and AQP5 proteins were preferentially expressed in endothelial cells, showing a higher intensity for AQP1 (66.7% of cases with an intensity of 3, and 93.3% of subjects with an extension of 3 among patients with COPD). Subtle interstitial disease was associated with type II pneumocyte hyperplasia and an increased expression of AQP1.ConclusionsThis study provides pilot observations on the differences in AQP1 and AQP5 expression between COPD patients and COPD-resistant smokers. Our findings suggest a potential role for AQP1 in the pathogenesis of COPD.

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“…Studies by the Verkman group, employing genetic knock-down of aquaporins, revealed a minor contribution of the transcellular, and therefore TJ independent pathway, on transepithelial water transport in the lung [83, 84, 114, 130, 131], suggesting a major contribution of TJ-dependent paracellular water flux to overall transepithelial water flux. However, other studies found that perturbations of aquaporin activity disturb transepithelial water transport and volume homeostasis in the airways [2, 32, 35, 113, 127], suggesting that TJ-independent water transport pathways through aquaporins contribute significantly to fluid transport across the airway epithelium. A more recent study now suggests that both processes occur in a different manner, where basal water transport activity is dominated by a paracellular pathway, whereas a compensatively increased water resorption is predominantly carried by an aquaporin-dependent transcellular pathway [110].…”

Section: Caludins Of the Alveolar And Airway Epitheliummentioning

confidence: 99%

Tight junctions in pulmonary epithelia during lung inflammation

Wittekindt

2016

Pflugers Arch - Eur J Physiol

174

131

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Inflammatory lung diseases like asthma bronchiale, chronic obstructive pulmonary disease and allergic airway inflammation are widespread public diseases that constitute an enormous burden to the health systems. Mainly classified as inflammatory diseases, the treatment focuses on strategies interfering with local inflammatory responses by the immune system. Inflammatory lung diseases predispose patients to severe lung failures like alveolar oedema, respiratory distress syndrome and acute lung injury. These life-threatening syndromes are caused by increased permeability of the alveolar and airway epithelium and exudate formation. However, the mechanism underlying epithelium barrier breakdown in the lung during inflammation is elusive. This review emphasises the role of the tight junction of the airway epithelium as the predominating structure conferring epithelial tightness and preventing exudate formation and the impact of inflammatory perturbations on their function.

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Anti-asthmatic agents alleviate pulmonary edema by upregulating AQP1 and AQP5 expression in the lungs of mice with OVA-induced asthma

Cited by 57 publications

References 34 publications

Effects of glucocorticoid on the expression and regulation of aquaporin 5 in the paranasal sinus of rats with chronic rhinosinusitis

Effects of glucocorticoid on the expression and regulation of aquaporin 5 in the paranasal sinus of rats with chronic rhinosinusitis

Expression of aquaporins in bronchial tissue and lung parenchyma of patients with chronic obstructive pulmonary disease

Tight junctions in pulmonary epithelia during lung inflammation

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