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Study on the Role and Mechanism of Aquaporin 3 in Pulmonary Infection Caused by Pseudomonas Aeruginosa
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A7629 - Study on the Role and Mechanism of Aquaporin 3 in Pulmonary Infection Caused by Pseudomonas Aeruginosa
Author Block: M. Chang; Zhongshan Hospital, Shanghai, China.
Rational: To investigate the role and mechanism of aquaporin 3 (AQP3) in pulmonary infection caused by Pseudomonas aeruginosa (PAO1).Methods: We established the pulmonary infection model in mice by PAO1 airway infusion. The expression level of mRNA and protein of AQP3 in lung tissue were detected by PCR and Western Blot at 24h, 48h and 72h after infection. For further study, the 72h-pulmonary infection model was established on wild type (WT) and AQP3 knockout (AQP3-/-) mice in the same way. We observed the histological characteristics, total protein and cells count in BALF and so on to compare the lung injury of the two groups. In addition, the AQP3 knockdown virus vector was constructed to detect the effect of AQP3 knockdown on genes and proteins related to proliferation in order to study the downstream signaling pathways of AQP3. Results: Pulmonary infection caused by PAO1 could increase the expression level of AQP3 mRNA and protein at 24 h, 48 h and 72 h, and the difference was significant at 72 h compared with PBS control. At 72h, the pulmonary infection caused by PAO1 induced inflammation in both WT and AQP3-/- groups and the extent of inflammatory infiltration in PAO1/AQP3-/- was significantly more severe than PAO1/WT group by HE staining observation. Also the total protein concentration in BALF of WT and AQP3-/- groups were significantly increased and the level is higher in PAO1/AQP3-/- compared to PAO1/WT group. AQP3 knockdown virus vectors shAQP3-1 and shAQP3-2 significantly decreased the expression of AQP3 in lung epithelial cells, so as to significantly inhibit the expression of Survivin and cyclin-dependent kinase (CDK1). Conclusion: In this study, it was observed that AQP3 was overexpressed in the lung of mouse infected with PAO1 and may protect the airway epithelial cells (AECs) through Survivin and CDK1 signaling pathway in pulmonary infection. These results imply a critical role of AQP3 in pulmonary infection, and AQP3 may be a novel therapeutic target.
Author Block: M. Chang; Zhongshan Hospital, Shanghai, China.
Rational: To investigate the role and mechanism of aquaporin 3 (AQP3) in pulmonary infection caused by Pseudomonas aeruginosa (PAO1).Methods: We established the pulmonary infection model in mice by PAO1 airway infusion. The expression level of mRNA and protein of AQP3 in lung tissue were detected by PCR and Western Blot at 24h, 48h and 72h after infection. For further study, the 72h-pulmonary infection model was established on wild type (WT) and AQP3 knockout (AQP3-/-) mice in the same way. We observed the histological characteristics, total protein and cells count in BALF and so on to compare the lung injury of the two groups. In addition, the AQP3 knockdown virus vector was constructed to detect the effect of AQP3 knockdown on genes and proteins related to proliferation in order to study the downstream signaling pathways of AQP3. Results: Pulmonary infection caused by PAO1 could increase the expression level of AQP3 mRNA and protein at 24 h, 48 h and 72 h, and the difference was significant at 72 h compared with PBS control. At 72h, the pulmonary infection caused by PAO1 induced inflammation in both WT and AQP3-/- groups and the extent of inflammatory infiltration in PAO1/AQP3-/- was significantly more severe than PAO1/WT group by HE staining observation. Also the total protein concentration in BALF of WT and AQP3-/- groups were significantly increased and the level is higher in PAO1/AQP3-/- compared to PAO1/WT group. AQP3 knockdown virus vectors shAQP3-1 and shAQP3-2 significantly decreased the expression of AQP3 in lung epithelial cells, so as to significantly inhibit the expression of Survivin and cyclin-dependent kinase (CDK1). Conclusion: In this study, it was observed that AQP3 was overexpressed in the lung of mouse infected with PAO1 and may protect the airway epithelial cells (AECs) through Survivin and CDK1 signaling pathway in pulmonary infection. These results imply a critical role of AQP3 in pulmonary infection, and AQP3 may be a novel therapeutic target.
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