title: Altered regulation of aquaporin gene expression in allergen and IL-13-induced mouse models of asthma.
abstract: IL-13 is known to affect many processes that contribute to an asthmatic phenotype, including inflammation, fibrosis, and mucus production. Members of the aquaporin (AQP) family of transmembrane water channels are targets of regulation in models of lung injury and inflammation. Therefore, we examined AQP mRNA and protein expression in allergen and IL-13-induced mouse models of asthma. Lungs from ovalbumin sensitized and ovalbumin challenged (OVA/OVA) and IL-13 treated mice showed airway thickening, increased mucus production, and pulmonary eosinophilia. Pulmonary function tests showed a significant increase in methacholine-induced airway hyperreactivity in OVA/OVA and IL-13-treated mice as compared with controls. Quantitative PCR analysis revealed differential regulation of AQPs in these two models. AQP1 and AQP4 mRNA expression was downregulated in the OVA/OVA model, but not in the IL-13 model. AQP5 mRNA was reduced in both models, whereas AQP3 was upregulated only in the IL-13 model. Western analysis showed that diminished expression of an apically localized aquaporin, (AQP5), and concomitant upregulation of a basolateral aquaporin (AQP3 or AQP4) are characteristic features of both inducible asthma models. These results demonstrate that aquaporins are common targets of gene expression in both allergen and IL-13 induced mouse models of asthma.
authors.affiliation: Department of Biology, University of Dayton, 300 College Park, Dayton, OH 45469, USA. Carissa.Krane@notes.udayton.edu
authors.forename: Carissa M
authors.initials: CM
authors.lastname: Krane
authors.forename: Bijia
authors.initials: B
authors.lastname: Deng
authors.forename: Venkateshwar
authors.initials: V
authors.lastname: Mutyam
authors.forename: Casey A
authors.initials: CA
authors.lastname: McDonald
authors.forename: Stephen
authors.initials: S
authors.lastname: Pazdziorko
authors.forename: Lawrence
authors.initials: L
authors.lastname: Mason
authors.forename: Samuel
authors.initials: S
authors.lastname: Goldman
authors.forename: Marion
authors.initials: M
authors.lastname: Kasaian
authors.forename: Divya
authors.initials: D
authors.lastname: Chaudhary
authors.forename: Cara
authors.initials: C
authors.lastname: Williams
authors.forename: Melisa W Y
authors.initials: MW
authors.lastname: Ho
mesh_terms: D000818:Animals; D051398:Aquaporin 1 / Q000096:biosynthesis; D051401:Aquaporin 4 / Q000096:biosynthesis; D051402:Aquaporin 5 / Q000096:biosynthesis* / Q000378:metabolism*; D001249:Asthma / Q000378:metabolism*; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D005786:Gene Expression Regulation; D007249:Inflammation; D018793:Interleukin-13 / Q000096:biosynthesis*; D008168:Lung / Q000378:metabolism; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D008954:Models, Biological
chemical_list: D051401:Aquaporin 4; D051402:Aquaporin 5; D016085:Bronchoconstrictor Agents; D018793:Interleukin-13; D016210:Methacholine Chloride; D051398:Aquaporin 1