Proteomic Analysis of Lung Tissue in a Rat Acute Lung Injury Model: Identification of PRDX1 as a Promoter of Inflammation

Author:

Liu Dongdong12,Mao Pu13,Huang Yongbo12,Liu Yiting12,Liu Xiaoqing12,Pang Xiaoqing12,Li Yimin12

Affiliation:

1. State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Guangzhou, Guangdong 510120, China

2. Intensive Care Unit, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

3. Infection Control Department, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

Abstract

Acute respiratory distress syndrome (ARDS) remains a high morbidity and mortality disease entity in critically ill patients, despite decades of numerous investigations into its pathogenesis. To obtain global protein expression changes in acute lung injury (ALI) lung tissues, we employed a high-throughput proteomics method to identify key components which may be involved in the pathogenesis of ALI. In the present study, we analyzed lung tissue proteomes ofPseudomonas aeruginosa-induced ALI rats and identified eighteen proteins whose expression levels changed more than twofold as compared to normal controls. In particular, we found that PRDX1 expression in culture medium was elevated by a lipopolysaccharide (LPS) challenge in airway epithelial cellsin vitro. Furthermore, overexpression of PRDX1 increased the expression of proinflammatory cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α(TNF-α), whereas knockdown of PRDX1 led to downregulated expression of cytokines induced by LPS. In conclusion, our findings provide a global alteration in the proteome of lung tissues in the ALI rat model and indicate that PRDX1 may play a critical role in the pathogenesis of ARDS by promoting inflammation and represent a novel strategy for the development of new therapies against ALI.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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