Expression and function of aquaporin-1 in hyperoxia‑exposed alveolar epithelial type Ⅱ cells

Zhang,Qiu-Yue; Fu,Jian-Hua; Xue,Xin-Dong

doi:10.3892/etm.2014.1739

Expression and function of aquaporin-1 in hyperoxia‑exposed alveolar epithelial type Ⅱ cells

Authors:
- Qiu-Yue Zhang
- Jian-Hua Fu
- Xin-Dong Xue
View Affiliations

Affiliations: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China
Published online on: May 28, 2014 https://doi.org/10.3892/etm.2014.1739
Pages: 493-498

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The aim of the present study was to investigate water transport dysfunction in alveolar epithelial type II cells (AECII), which were exposed to hyperoxia, and to investigate the mechanism of pulmonary edema resulting from hyperoxic lung injury. The lung cells of newborn rats were isolated for primary cell culture and divided into control and experimental groups. The control and experimental group cells were placed into a normoxic incubator (oxygen volume fraction, 0.21) or hyperoxic incubator (oxygen volume fraction, 0.9), respectively. Twenty‑four, 48 and 72 h after cell attachment, the gene transcription and protein expression levels of aquaporin‑1 (AQP1) were detected via quantitative polymerase chain reaction and western blot analysis. Flow cytometry was conducted to detect the volume of the cells in the experimental and control groups. In the present study, it was identified that AQP1 expression and cell volume were greater in the experimental group when compared with the control group. Thus, hyperoxia may disturb the gene expression regulation of AQP1 in AECII, resulting in water transport dysfunction. This may be one of the mechanisms underlying pulmonary edema caused by hyperoxic lung injury.

View Figures

View References

1	Itoh T, Rai T, Kuwahara M, et al: Identification of a novel aquaporin, AQP12, expressed in pancreatic acinar cells. Biochem Biophys Res Commun. 330:832–838. 2005. View Article : Google Scholar : PubMed/NCBI
2	Borok Z and Verkman AS: Lung edema clearance: 20 years of progress: invited review: role of aquaporin water channls in fluid transport in lung and airways. J Appl Physiol (1985). 93:2199–2206. 2002.PubMed/NCBI
3	Kreda SM, Gynn MC, Fenstermacher DA, et al: Expression and localization of epithelial aquaporins in the adult human lung. Am J Respir Cell Mol Biol. 24:224–234. 2001. View Article : Google Scholar : PubMed/NCBI
4	Agre P and Kozono D: Aquaporin water channels: molecular mechanisms for human diseases. FEBS Lett. 555:72–78. 2003. View Article : Google Scholar : PubMed/NCBI
5	Ma T, Fukuda N, Song Y, et al: Lung fluid transport in aquaporin-5 knockout mice. J Clin Invest. 105:93–100. 2000. View Article : Google Scholar
6	Ruddy MK, Drazen JM, Pitkanen OM, Rafii B, O’Brodovich HM and Harris HW: Modulation of aquaporin 4 and the amiloride-inhibitable sodium channel in perinatal rat lung epithelial cells. Am J Physiol. 274:L1066–L1072. 1998.PubMed/NCBI
7	Zelenina M, Zelenin S and Aperia A: Water channels (aquaporins) and their role for postnatal adaptation. Pediatr Res. 57:47R–53R. 2005. View Article : Google Scholar : PubMed/NCBI
8	King LS, Nielsen S, Agre P and Brown RH: Decreased pulmonary vascular permeability in aquaporin-1-null humans. Proc Natl Acad Sci USA. 99:1059–1063. 2002. View Article : Google Scholar : PubMed/NCBI
9	Song Y, Ma T, Matthay MA and Verkman AS: Role of aquaporin-4 in airspace-to-capillary water permeability in intact mouse lung measured by a novel gravimetric method. J Gen Physiol. 115:17–27. 2000. View Article : Google Scholar : PubMed/NCBI
10	Bai C, Fukuda N, Song Y, Ma T, Matthay MA and Verkman AS: Lung fluid transport in aquaporin-1 and aquaporin-4 knockout mice. J Clin Invest. 103:555–561. 1999. View Article : Google Scholar : PubMed/NCBI
11	Wang L, Maher TJ and Wurtman RJ: Oral L-glutamine increases GABA levels in striatal tissue and extracellular fluid. FASEB J. 21:1227–1232. 2007. View Article : Google Scholar : PubMed/NCBI
12	Franco-Montoya ML, Bourbon JR, Durrmeyer X, Lorotte S, Jarreau PH and Delacourt C: Pulmonary effects of keratinocyte growth factor in newborn rats exposed to hyperoxia. Am J Physiol Lung Cell Mol Physiol. 297:L965–L976. 2009. View Article : Google Scholar : PubMed/NCBI
13	Modi N: Clinical implications of postnatal alterations in body water distribution. Semin Neonatol. 8:301–306. 2003. View Article : Google Scholar : PubMed/NCBI
14	Verkman AS: Role of aquaporins in lung liquid physiology. Respir Physiol Neurobiol. 159:324–330. 2007. View Article : Google Scholar : PubMed/NCBI
15	Lecuona E, Trejo HE and Sznajder JI: Regulation of Na, K-ATPase during acute lung injury. J Bioenerg Biomembr. 39:391–395. 2007. View Article : Google Scholar : PubMed/NCBI
16	Dobbs LG, Gonzalez R and Williams MC: An improved method for isolating type II cells in high yield and purity. Am Rev Respir Dis. 134:141–145. 1986.PubMed/NCBI
17	Jordan CT, Yamasaki G and Minamoto D: High-resolution cell cycle analysis of defined phenotypic subsets within primitive human hematopoietic cell populations. Exp Hematol. 24:1347–1355. 1996.PubMed/NCBI
18	Yue DM, Tong YJ and Xue XD: Ultrastructure changes of alveolar epithelial type II cells in newborn rats with chronic lung disease induced by hyperoxia. J Appl Clin Pediatr. 26:691–693. 2011.(In Chinese).
19	Tsushima K, King LS, Aggarwal NR, De Gorordo A, D’Alessio FR and Kubo K: Acute lung injury review. Intern Med. 48:621–630. 2009. View Article : Google Scholar
20	Krane CM, Deng B, Mutyam V, et al: Altered Regulation of aquaporin gene expression in allergen and IL-13-induced mouse models of asthma. Cytokine. 46:111–118. 2009. View Article : Google Scholar : PubMed/NCBI
21	King LS and Agre P: Pathophysiology of the aquaporin water channels. Annu Rev Physiol. 58:619–648. 1996. View Article : Google Scholar : PubMed/NCBI
22	Wu XM, Wang HY, Li GF, Zang B and Chen WM: Dobutamine enhances alveolar fluid clearance in a rat model of acute lung injury. Lung. 187:225–231. 2009. View Article : Google Scholar : PubMed/NCBI
23	Schweitzer K, Li E, Sidhaye V, Leitch V, Kuznetsov S and King LS: Accumulation of aquaporin-1 during hemolysin-induced necrotic cell death. Cell Mol Biol Lett. 13:195–211. 2008. View Article : Google Scholar : PubMed/NCBI
24	Towne JE, Harrod KS, Krane CM and Menon AG: Decreased expression of aquaporin (AQP)1 and AQP5 in mouse lung after acute viral infection. Am J Respir Cell Mol Biol. 22:34–44. 2000. View Article : Google Scholar : PubMed/NCBI
25	Botto L, Beretta E, Daffara R, Miserocchi G and Palestini P: Biochemical and morphological changes in endothelial cells in response to hypoxic interstitial edema. Respir Res. 7:72006. View Article : Google Scholar : PubMed/NCBI
26	Wang F, Huang H, Lu F and Chen Y: Acute lung injury and change in expression of aquaporins 1 and 5 in a rat model of acute pancreatitis. Hepatogastroenterology. 57:1553–1562. 2010.PubMed/NCBI
27	Lai KN, Leung JC, Metz CN, Lai FM, Bucala R and Lan HY: Role for macrophage migration inhibitory factor in acute respiratory distress syndrome. J Pathol. 199:496–508. 2003. View Article : Google Scholar : PubMed/NCBI
28	Li J, Xu M, Fan Q, et al: Tanshinone IIA ameliorates seawater exposure-induced lung injury by inhibiting aquaporins (AQP) 1 and AQP5 expression in lung. Respir Physiol Neurobiol. 176:39–49. 2011. View Article : Google Scholar : PubMed/NCBI
29	Song Y, Fukuda N, Bai C, Ma T, Matthay MA and Verkman AS: Role of aquaporins in alveolar fluid clearance in neonatal and adult lung, and in oedema formation following acute lung injury: studies in transgenic aquaporin null mice. J Physiol. 525:771–779. 2000. View Article : Google Scholar : PubMed/NCBI
30	Tsai CL, Lin YC, Wang HM and Chou TC: Baicalein, an active component of Scutellaria baicalensis, protects against lipopolysaccharide-induced acute lung injury in rats. J Ethnopharmacol. View Article : Google Scholar
31	Huang CS, Kawamura T, Peng X, et al: Hydrogen inhalation reduced epithelial apoptosis in ventilator-induced lung injury via a mechanism involving nuclear factor-kappa B activation. Biochem Biophys Res Commun. 408:253–258. 2011. View Article : Google Scholar
32	McCoy E and Sontheimer H: MAPK induces AQP1 expression in astrocytes following injury. Glia. 58:209–217. 2010. View Article : Google Scholar : PubMed/NCBI
33	Maruyama T, Kadowaki H, Okamoto N, et al: CHIP-dependent termination of MEKK2 regulates temporal ERK activation required for proper hyperosmotic response. EMBO J. 29:2501–2514. 2010. View Article : Google Scholar : PubMed/NCBI
34	Zhang Z, Chen Z, Song Y, Zhang P, Hu J and Bai C: Expression of aquaporin 5 increases proliferation and metastasis potential of lung cancer. J Pathol. 221:210–220. 2010. View Article : Google Scholar : PubMed/NCBI
35	Lee MD, King LS, Nielsen S and Agre P: Genomic organization and developmental expression of aquaporin-5 in lung. Chest. 111(6 Suppl): 111S–113S. 1997. View Article : Google Scholar : PubMed/NCBI