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Int. J. Mol. Sci. 2016, 17(7), 1183;

The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome

Department of Anesthesiology, the Sixth People’s Hospital, Shanghai Jiao Tong University, Shanghai 200233, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Kenichi Ishibashi
Received: 4 June 2016 / Revised: 11 July 2016 / Accepted: 15 July 2016 / Published: 21 July 2016
(This article belongs to the Special Issue Aquaporin)
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This study was designed to investigate the role of aquaporin1 (AQP1) in the pathologic process of pulmonary edema induced by fat embolism syndrome (FES) and the effects of a free fatty acid (FFA) mixture on AQP1 expression in pulmonary microvascular endothelial cells (PMVECs). In vivo, edema was more serious in FES mice compared with the control group. The expression of AQP1 and the wet-to-dry lung weight ratio (W/D) in the FES group were significantly increased compared with the control group. At the same time, inhibition of AQP1 decreased the pathological damage resulting from pulmonary edema. Then we performed a study in vitro to investigate whether AQP1 was induced by FFA release in FES. The mRNA and protein level of AQP1 were increased by FFAs in a dose- and time-dependent manner in PMVECs. In addition, the up-regulation of AQP1 was blocked by the inhibitor of p38 kinase, implicating the p38 MAPK pathway as involved in the FFA-induced AQP1 up-regulation in PMVECs. Our results demonstrate that AQP1 may play important roles in pulmonary edema induced by FES and can be regarded as a new therapy target for treatment of pulmonary edema induced by FES. View Full-Text
Keywords: AQP1; fat embolism syndrome; pulmonary edema; free fatty acid; p38 MAPK signaling pathway AQP1; fat embolism syndrome; pulmonary edema; free fatty acid; p38 MAPK signaling pathway

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Zhang, Y.; Tian, K.; Wang, Y.; Zhang, R.; Shang, J.; Jiang, W.; Wang, A. The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome. Int. J. Mol. Sci. 2016, 17, 1183.

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