Changes in water channel aquaporin 1 and aquaporin 5 in the small airways and the alveoli in a rat asthma model

Abduxukur Ablimit, Bilal Hasan, Wenju Lu, Wen Qin, Qimanguli Wushouer, Nanshan Zhong, Halmurat Upur

Research output: Contribution to journalArticle

Abstract

Objectives: To examine changes in aquaporin 1 (AQP1) and aquaporin 5 (AQP5) in the small airways and alveoli in a rat asthma model. Method: Forty Wistar rats were randomly divided into a control group and an ovalbumin (OVA) sensitization asthma model group. The distribution and expression of AQP1 and AQP5 in lung tissues were analyzed using immunohistochemistry (IHC), quantified the staining intensity by assessing integrated optical densities (IOD), and Western blotting (WB). Results: IHC showed AQP1 was mainly distributed in sub-epithelial microvascular endothelial cells (MECs) and red blood cells. IOD values showed, in the asthma model group, the expression of AQP1 in alveolar MECs was lower than that in the control group (P<0.05); However, AQP1 expression in small airways sub-epithelial was higher than in the control group (P<0.05). The WB indicated that AQP1 expression in the asthma model group was 57% lower than in the control group (P<0.05). AQP5 was mainly distributed in the non-ciliated epithelial cells of the small airways and the apical membranes of type I and type II epithelial cells. IOD values showed, in asthma model group, the expression of AQP5 increased in small airways epithelium (P<0.05), and decreased in alveolar epithelium (P<0.05). The WB showed a 36% reduction in AQP5 expression compared with the control group (P<0.05). Conclusion: AQP1 and AQP5 increased in small airways in rats with experimentally induced asthma, indicating that they may be involved in the formation of submucosal edema and mucus hypersecretion. Decreased AQP1 and AQP5 in pulmonary alveoli may be related to increased alveolar liquid viscosity and the formation of mucus plugs.

Original languageEnglish (US)
Pages (from-to)68-73
Number of pages6
JournalMicron
Volume45
DOIs
StatePublished - Feb 2013
Externally publishedYes

Fingerprint

Aquaporin 5
Aquaporin 1
Aquaporins
Asthma
Control Groups
Western Blotting
Mucus
Epithelium
Pulmonary Alveoli
Endothelial Cells
Epithelial Cells
Immunohistochemistry
Ovalbumin
Viscosity
Wistar Rats
Edema
Erythrocytes
Staining and Labeling

Keywords

  • Aquaporin
  • Hypersecretion
  • Rat asthma model

ASJC Scopus subject areas

  • Cell Biology
  • Structural Biology

Cite this

Changes in water channel aquaporin 1 and aquaporin 5 in the small airways and the alveoli in a rat asthma model. / Ablimit, Abduxukur; Hasan, Bilal; Lu, Wenju; Qin, Wen; Wushouer, Qimanguli; Zhong, Nanshan; Upur, Halmurat.

In: Micron, Vol. 45, 02.2013, p. 68-73.

Research output: Contribution to journalArticle

Ablimit, Abduxukur ; Hasan, Bilal ; Lu, Wenju ; Qin, Wen ; Wushouer, Qimanguli ; Zhong, Nanshan ; Upur, Halmurat. / Changes in water channel aquaporin 1 and aquaporin 5 in the small airways and the alveoli in a rat asthma model. In: Micron. 2013 ; Vol. 45. pp. 68-73.
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abstract = "Objectives: To examine changes in aquaporin 1 (AQP1) and aquaporin 5 (AQP5) in the small airways and alveoli in a rat asthma model. Method: Forty Wistar rats were randomly divided into a control group and an ovalbumin (OVA) sensitization asthma model group. The distribution and expression of AQP1 and AQP5 in lung tissues were analyzed using immunohistochemistry (IHC), quantified the staining intensity by assessing integrated optical densities (IOD), and Western blotting (WB). Results: IHC showed AQP1 was mainly distributed in sub-epithelial microvascular endothelial cells (MECs) and red blood cells. IOD values showed, in the asthma model group, the expression of AQP1 in alveolar MECs was lower than that in the control group (P<0.05); However, AQP1 expression in small airways sub-epithelial was higher than in the control group (P<0.05). The WB indicated that AQP1 expression in the asthma model group was 57{\%} lower than in the control group (P<0.05). AQP5 was mainly distributed in the non-ciliated epithelial cells of the small airways and the apical membranes of type I and type II epithelial cells. IOD values showed, in asthma model group, the expression of AQP5 increased in small airways epithelium (P<0.05), and decreased in alveolar epithelium (P<0.05). The WB showed a 36{\%} reduction in AQP5 expression compared with the control group (P<0.05). Conclusion: AQP1 and AQP5 increased in small airways in rats with experimentally induced asthma, indicating that they may be involved in the formation of submucosal edema and mucus hypersecretion. Decreased AQP1 and AQP5 in pulmonary alveoli may be related to increased alveolar liquid viscosity and the formation of mucus plugs.",
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AU - Ablimit, Abduxukur

AU - Hasan, Bilal

AU - Lu, Wenju

AU - Qin, Wen

AU - Wushouer, Qimanguli

AU - Zhong, Nanshan

AU - Upur, Halmurat

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AB - Objectives: To examine changes in aquaporin 1 (AQP1) and aquaporin 5 (AQP5) in the small airways and alveoli in a rat asthma model. Method: Forty Wistar rats were randomly divided into a control group and an ovalbumin (OVA) sensitization asthma model group. The distribution and expression of AQP1 and AQP5 in lung tissues were analyzed using immunohistochemistry (IHC), quantified the staining intensity by assessing integrated optical densities (IOD), and Western blotting (WB). Results: IHC showed AQP1 was mainly distributed in sub-epithelial microvascular endothelial cells (MECs) and red blood cells. IOD values showed, in the asthma model group, the expression of AQP1 in alveolar MECs was lower than that in the control group (P<0.05); However, AQP1 expression in small airways sub-epithelial was higher than in the control group (P<0.05). The WB indicated that AQP1 expression in the asthma model group was 57% lower than in the control group (P<0.05). AQP5 was mainly distributed in the non-ciliated epithelial cells of the small airways and the apical membranes of type I and type II epithelial cells. IOD values showed, in asthma model group, the expression of AQP5 increased in small airways epithelium (P<0.05), and decreased in alveolar epithelium (P<0.05). The WB showed a 36% reduction in AQP5 expression compared with the control group (P<0.05). Conclusion: AQP1 and AQP5 increased in small airways in rats with experimentally induced asthma, indicating that they may be involved in the formation of submucosal edema and mucus hypersecretion. Decreased AQP1 and AQP5 in pulmonary alveoli may be related to increased alveolar liquid viscosity and the formation of mucus plugs.

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