Decreased Expression of Aquaporin (AQP)1 and AQP5 in Mouse Lung after Acute Viral Infection

Towne, Jennifer E.; Harrod, Kevin S.; Krane, Carissa M.; Menon, Anil G.

doi:10.1165/ajrcmb.22.1.3818

Cited by 187 publications

(160 citation statements)

References 37 publications

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“…At the alveolar level, AQP1 and AQP5 are the most abundant, with an endothelial or epithelial distribution, respectively (35,36). It has been shown that AQP5 knockout mice develop less inflammation in a model of house dust miteinduced asthma (37).…”

Section: Discussionmentioning

confidence: 99%

Critical Role of Aquaporins in Interleukin 1β (IL-1β)-induced Inflammation

Rabolli

Wallemme

et al. 2014

Journal of Biological Chemistry

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Background: Aquaporins are channels permeable to water, and they are essential for immune cell migration. Results: We demonstrate that aquaporin-mediated water fluxes are necessary for the NLRP3 inflammasome-dependent release of mature IL-1␤ in vitro and in vivo. Conclusion: Aquaporins are implicated in the mechanisms of proinflammatory cytokine secretion during inflammation. Significance: The discovery of a new function for AQPs opens new diagnostic and therapeutic opportunities in inflammatory disorders.

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Section: Discussionmentioning

confidence: 99%

Critical Role of Aquaporins in Interleukin 1β (IL-1β)-induced Inflammation

Rabolli

Wallemme

et al. 2014

Journal of Biological Chemistry

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“…5 g of each RNA sample was converted to cDNA in a total volume of 21 l, using the SuperScript first-strand synthesis system for RT-PCR (Invitrogen). cDNA products were amplified by PCR using the following gene-specific primers: IFN-␥ (5Ј-TGGCTGTTTCT-GGCTGTTACTG-3Ј and 5Ј-AATCAGCAGCGACTCCTTTTCC-3Ј) (24), IL-1␤ (5Ј-TGACGGACCCCAAAAGATGAAG-3Ј and 5Ј-CTGCTTGTGA-GGTGCTGATGTA-3Ј) (25), IL-18 (5Ј-GGCCCAGGAACAATGGCTGC-C-3Ј and 5Ј-GGGTCACAGCCAGTCCTCTTAC-3Ј) (26), IL-12p40 (5Ј-A-GATGACATCACCTGGACCT-3Ј and 5Ј-GCCATGAGCACGTGAACCG-T-3Ј) (26), transforming growth factor-␤ (5Ј-GCGGACTACTATGCTAA-AGAGG-3Ј and 5Ј-GTTGTGTTGGTTGTAGAGGGCA-3Ј) (24), and ␤-actin (5Ј-ATGTACGTAGCCATCCAGGC-3Ј and 5Ј-AAGGAAGGCTGG-AAAAGAGC-3Ј) (27). PCR conditions were as follows: 94°C for 2 min and then 30 cycles at 94°C for 30 s, 58°C (IL-1␤ and ␤-actin) or 60°C (IFN-␥, IL-18, IL-12p40, transforming growth factor-␤) for 1 min, and 72°C for 1 min, followed by 72°C for 10 min.…”

Section: Methodsmentioning

confidence: 99%

In Vivo Evidence for Interferon-γ-mediated Homeostatic Mechanisms in Small Intestine of the NHE3 Na+/H+ Exchanger Knockout Model of Congenital Diarrhea

Woo¹,

Gildea²,

Tack³

et al. 2002

Journal of Biological Chemistry

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Mice lacking NHE3, the major absorptive Na ؉ /H ؉ exchanger in the intestine, are the only animal model of congenital diarrhea. To identify molecular changes underlying compensatory mechanisms activated in chronic diarrheas, cDNA microarrays and Northern blot analyses were used to compare global mRNA expression patterns in small intestine of NHE3-deficient and wildtype mice. Among the genes identified were members of the RegIII family of growth factors, which may contribute to the increased absorptive area, and a large number of interferon-␥-responsive genes. The latter finding is of particular interest, since interferon-␥ has been shown to regulate ion transporter activities in intestinal epithelial cells. Serum interferon-␥ was elevated 5-fold in NHE3-deficient mice; however, there was no evidence of inflammation, and unlike conditions such as inflammatory bowel disease, levels of other cytokines were unchanged. In addition, quantitative PCR analysis showed that up-regulation of interferon-␥ mRNA was localized to the small intestine and did not occur in the colon, spleen, or kidney. These in vivo data suggest that elevated interferon-␥, produced by gut-associated lymphoid tissue in the small intestine, is part of a homeostatic mechanism that is activated in response to the intestinal absorptive defect in order to regulate the fluidity of the intestinal tract.

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“…Mouse lungs from 12-weekold sex-matched Aqp5 ϩ/ϩ and Aqp5 Ϫ/Ϫ littermates were inflation-fixed in phosphate buffered 4% paraformaldehyde, paraffin-embedded, and sectioned at 5 m. Immunohistochemical staining was evaluated as described (4), by using a peptidederived, monospecific rabbit polyclonal antibody raised against the mouse͞rat AQP5 C-terminal peptide sequence (LL639; 0.5 g͞ml; ref. 13) and a Vectastain ABC Peroxidase Elite AntiRabbit IgG kit (Vector Laboratories, Burlingame, CA) to detect the antigen:antibody complexes.…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies have explored the regulation of Aqp5 gene expression in normal and disease states. In a mouse model of acute lung injury, AQP5 mRNA and protein expression were significantly decreased in association with pulmonary inflammation and edema resulting from adenoviral infection (4). Moreover, AQP5 expression in a murine lung epithelial cell line (MLE-12) is modulated by the proinf lammatory cytokine TNF-␣ through an nuclear factor (NF)-B-dependent pathway (5).…”

mentioning

confidence: 99%

Aquaporin 5-deficient mouse lungs are hyperresponsive to cholinergic stimulation

Krane

Fortner

Hand

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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106

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Although aquaporin 5 (AQP5) is the major water channel expressed in alveolar type I cells in the lung, its actual role in the lung is a matter of considerable speculation. By using immunohistochemical staining, we show that AQP5 expression in mouse lung is not restricted to type I cells, but is also detected in alveolar type II cells, and in tracheal and bronchial epithelium. Aqp5 knockout (Aqp5 ؊/؊ ) mice were used to analyze AQP5 function in pulmonary physiology. Compared with Aqp5 ؉/؉ mice, Aqp5 ؊/؊ mice show a significantly increased concentration-dependent bronchoconstriction to intravenously administered Ach, as shown by an increase in total lung resistance and a decrease in dynamic lung compliance (P < 0.05). Likewise, Penh, a measure of bronchoconstriction, was significantly enhanced in Aqp5 ؊/؊ mice challenged with aerosolized methacholine (P < 0.05). The hyperreactivity to bronchoconstriction observed in the Aqp5 ؊/؊ mice was not due to differences in tracheal smooth muscle contractility in isolated preparations or to altered levels of surfactant protein B. These data suggest a novel pathway by which AQP5 influences bronchoconstriction. This observation is of special interest because studies to identify genetic loci involved in airway hyperresponsiveness associated with asthma bracket genetic intervals on human chromosome 12q and mouse chromosome 15, which contain the Aqp5 gene.A quaporin 5 (AQP5) is a mercury-sensitive water channel expressed in mouse salivary gland acinar cells, alveolar type I cells, lacrimal glands, and the eye (1-3). However, the function of AQP5 in mouse lung physiology and pathophysiology is largely unknown. Recent studies have explored the regulation of Aqp5 gene expression in normal and disease states. In a mouse model of acute lung injury, AQP5 mRNA and protein expression were significantly decreased in association with pulmonary inflammation and edema resulting from adenoviral infection (4). Moreover, AQP5 expression in a murine lung epithelial cell line (MLE-12) is modulated by the proinf lammatory cytokine TNF-␣ through an nuclear factor (NF)-B-dependent pathway (5). Keratinocyte growth factor also has been shown to mediate the differentiation status of alveolar epithelial cells and AQP5 expression (6). However, a clear understanding of AQP5 function in the lung remains to be discerned.Previously published studies have addressed functional questions limited to the examination of the role of AQP5 in type I cells in fluid clearance and airspace-capillary osmotic water permeability. Of significance, isolated perfused lungs from Aqp5 Ϫ/Ϫ mice were shown to have a 10-fold reduction in airspace-capillary osmotic water permeability (7). Experiments addressing the role of AQP5 in alveolar fluid clearance failed to indicate a role for AQP5 in this process under certain physiological conditions (8). Based on the results of these studies, some have concluded that AQP5 does not play a major role in lung physiology. Contrary to these conclusions, the data reported here clearly define a...

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Decreased Expression of Aquaporin (AQP)1 and AQP5 in Mouse Lung after Acute Viral Infection

Cited by 187 publications

References 37 publications

Critical Role of Aquaporins in Interleukin 1β (IL-1β)-induced Inflammation

Critical Role of Aquaporins in Interleukin 1β (IL-1β)-induced Inflammation

In Vivo Evidence for Interferon-γ-mediated Homeostatic Mechanisms in Small Intestine of the NHE3 Na+/H+ Exchanger Knockout Model of Congenital Diarrhea

Aquaporin 5-deficient mouse lungs are hyperresponsive to cholinergic stimulation

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