Altered regulation of aquaporin gene expression in allergen and IL-13-induced mouse models of asthma

Krane, Carissa M.; Deng, Bijia; Mutyam, Venkateshwar; McDonald, C.A.; Pazdziorko, Stephen; Mason, Lawrence E.; Goldman, Samuel J.; Kasaian, Marion T.; Chaudhary, Divya; Williams, Cara; Ho, Melisa W-Y.

doi:10.1016/j.cyto.2008.12.018

Cited by 35 publications

(24 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inflammatory cytokines have been found to be involved in overproduction and overexpression of mucus proteins and genes in the airway epithelium [15, 16]. For example, Th2 cytokines like IL‐4 were suggested to regulate mucin gene expression [17] and were down‐regulated in the AQP5 KO mouse, suggesting that AQP5 may be involved in robust Th2‐driven responses to allergens.…”

Section: Discussionmentioning

confidence: 99%

Role of aquaporin 5 in antigen‐induced airway inflammation and mucous hyperproduction in mice

Shen

Wang

Chen

et al. 2011

J Cellular Molecular Medi

View full text Add to dashboard Cite

Airway inflammation and mucus hyperproduction play the central role in the development of asthma, although the mechanisms remain unclear. The aquaporin (AQP)-5 may be involved in the process due to its contribution to the volume of liquid secreted from the airways. The present study firstly found the overexpression of AQP5 in the airway epithelium and submucosal glands of asthmatics. Furthermore, we aimed at evaluating the role of AQP5 in airway inflammation and mucous hyperproductions during chronic allergic responses to house dust mite (HDM). Bronchoalveolar lavage levels of interleukin (IL)-2, IL-4, IL-10, interferon-γ and Mucin 5AC (MUC5AC), and number of peribronchial and perivascular cells were measured in AQP5 wild-type and AQP5 knockout (KO) mice. We found that HDM induced airway inflammation, lung Th2 cell accumulation and mucin hypersecretion in C57BL/6 mice rather than AQP5 KO mice. Expression of MUC5AC and MUC5B proteins and genes in the lung tissue was significantly lower in AQP5 KO mice. Thus, our results implicate involvement of AQP5 in the development of airway inflammation and mucous hyperproduction during chronic asthma.

show abstract

Section: Discussionmentioning

confidence: 99%

Role of aquaporin 5 in antigen‐induced airway inflammation and mucous hyperproduction in mice

Shen

Wang

Chen

et al. 2011

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…More recently, AQPs were described as potential downstream targets of altered gene expression in several murine models of induced asthma (by allergen ovalbumin or IL-13) (Krane et al, 2009 ). AQP3 and AQP5 gene expressions appear as quite early modification in the lung response to mIL-13 induced airway constriction.…”

Section: Potential Role Of Aquaporins In Different Models Of Inflammamentioning

confidence: 99%

New Perspectives on the Potential Role of Aquaporins (AQPs) in the Physiology of Inflammation

2018

View full text Add to dashboard Cite

Aquaporins (AQPs) are emerging, in the last few decades, as critical proteins regulating water fluid homeostasis in cells involved in inflammation. AQPs represent a family of ubiquitous membrane channels that regulate osmotically water flux in various tissues and sometimes the transport of small solutes, including glycerol. Extensive data indicate that AQPs, working as water channel proteins, regulate not only cell migration, but also common events essential for inflammatory response. The involvement of AQPs in several inflammatory processes, as demonstrated by their dysregulation both in human and animal diseases, identifies their new role in protection and response to different noxious stimuli, including bacterial infection. This contribution could represent a new key to clarify the dilemma of host-pathogen communications, and opens up new scenarios regarding the investigation of the modulation of specific AQPs, as target for new pharmacological therapies. This review provides updated information on the underlying mechanisms of AQPs in the regulation of inflammatory responses in mammals and discusses the broad spectrum of options that can be tailored for different diseases and their pharmacological treatment.

show abstract

“…In different lung fibrosis models, a loss of AQP-5 from alveolar epithelial cells has been described, thus indicating AQP-5 as an early injury marker in lung [32], [33]. The alveolar epithelium plays a central role in gas exchange and fluid transport, and is therefore critical for normal lung function.…”

Section: Resultsmentioning

confidence: 99%

Effect of P2X7 Receptor Knockout on AQP-5 Expression of Type I Alveolar Epithelial Cells

et al. 2014

View full text Add to dashboard Cite

P2X7 receptors, ATP-gated cation channels, are specifically expressed in alveolar epithelial cells. The pathophysiological function of this lung cell type, except a recently reported putative involvement in surfactant secretion, is unknown. In addition, P2X7 receptor-deficient mice show reduced inflammation and lung fibrosis after exposure with bleomycin. To elucidate the role of the P2X7 receptor in alveolar epithelial type I cells we characterized the pulmonary phenotype of P2X7 receptor knockout mice by using immunohistochemistry, western blot analysis and real-time RT PCR. No pathomorphological signs of fibrosis were found. Results revealed, however, a remarkable loss of aquaporin-5 protein and mRNA in young knockout animals. Additional in vitro experiments with bleomycin treated precision cut lung slices showed a greater sensitivity of the P2X7 receptor knockout mice in terms of aquaporin-5 reduction as wild type animals. Finally, P2X7 receptor function was examined by using the alveolar epithelial cell lines E10 and MLE-12 for stimulation experiments with bleomycin. The in vitro activation of P2X7 receptor was connected with an increase of aquaporin-5, whereas the inhibition of the receptor with oxidized ATP resulted in down regulation of aquaporin-5. The early loss of aquaporin-5 which can be found in different pulmonary fibrosis models does not implicate a specific pathogenetic role during fibrogenesis.

show abstract

Altered regulation of aquaporin gene expression in allergen and IL-13-induced mouse models of asthma

Cited by 35 publications

References 38 publications

Role of aquaporin 5 in antigen‐induced airway inflammation and mucous hyperproduction in mice

Role of aquaporin 5 in antigen‐induced airway inflammation and mucous hyperproduction in mice

New Perspectives on the Potential Role of Aquaporins (AQPs) in the Physiology of Inflammation

Effect of P2X7 Receptor Knockout on AQP-5 Expression of Type I Alveolar Epithelial Cells

Contact Info

Product

Resources

About