Journal
INJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED
Volume 43, Issue 8, Pages 1277-1283Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.injury.2012.04.004
Keywords
Pulmonary oedema; Epithelial sodium channel alpha subunit (alpha-ENaC); Insulin; Serum- and glucocorticoid-inducible; kinase-1 (SGK1); Lipopolysaccharide (LPS)
Funding
- National Natural Science Foundation of China [30971303]
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Activity of the epithelial sodium channels (ENaCs) in the lung tissue plays a critical role on sodium/fluid homeostasis and the lung fluid clearance. The serum-and glucocorticoid-inducible kinase-1 (SGK1), one of the critical regulation proteins of ENaC, is activated by insulin and growth factors possibly through 3-phosphoinositide-dependent kinase PDK1 or/and phosphatidylinositol 3-kinase (PI3K). However, it is uncertain whether insulin shows its stimulatory action on ENaC by activation of SGK1 in lipopolysaccharide (LPS)-induced acute lung injury (ALI) condition. In our study, Wistar rats were injected with LPS to induce ALI. Evans blue dye albumin (EBA) concentration was used to measure pulmonary oedema. For detecting the ratio of phospho-SGK1/SGK1 and alpha-ENaC protein, Western blot was performed. Real-time polymerase chain reaction (RT-PCR) was used to assess alpha-ENaC messenger RNA (mRNA). Immunohistochemistry was used to locate and quantitate alpha-ENaC expression. The EBA concentration was markedly increased by LPS alone but significantly reduced in rats that also received insulin injection. The ratio of phospho-SGK1/SGK1 was raised significantly in the insulin group and insulin + LPS group, compared with the control group and the LPS group, respectively. Furthermore, alpha-ENaC was up-regulated by insulin treatment. Simultaneously, injection with LPS significantly reduced alpha-ENaC expression. These findings demonstrated that insulin up-regulates ENaC in vivo possibly resulting from activation of SGK1. (C) 2012 Elsevier Ltd. All rights reserved.
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