期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 29, 期 2, 页码 599-606出版社
ELSEVIER
DOI: 10.1016/j.intimp.2015.09.022
关键词
Acute lung injury; HSPA12B; Endotoxemia; Vascular leakage; Inflammation
资金
- National Natural Science Foundation of China [81370260, 81371450, 81170321]
- Jiangsu Province's Outstanding Medical Academic Leader program [LJ201124]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Collaborative Innovation Center for Cardiovascular Disease Translational Medicine
Acute lung injury (ALI) is a critical manifestation of sepsis/septic shock. Heat shock protein A12B (HSPA12B), an endothelial cell-expressed heat shock protein, shows a negative regulation of lipopolysaccharide (LPS)-induced inflammation in myocardium and endothelial cells. However, it is unclear whether HSPA12B exerts protective effects against ALI during sepsis/septic shock. In this study, we treated HSPA12B transgenic mice (Tg) and wild type littermates (WT) with LPS for 6 h to induce endotoxemia. LPS treatment significantly caused pulmonary injuries as evidenced by microarchitecture destruction, vascular leakage and neutrophil recruitment in lungs of WT mice. However, the LPS-induced pulmonary injuries were significantly attenuated in Tg mice. Moreover, the LPS-induced activation of extracellular signal-regulated kinases (ERKs) and upregulation of intercellular adhesion molecule-1 (ICAM-1) and Cyclooxygenase-2 (Cox-2) were inhibited in Tg lungs compared with that in WT mice. Additionally, Tg lungs showed a significant lower level of vascular endothelial growth factor (VEGF) compared with WT mice. Our results demonstrate a pulmonary protective effect of HSPA12B against endotoxin challenge, which indicates management of HSPA12B expression could serve as a potential therapeutic target for ALI during sepsis/septic shock. (C) 2015 Elsevier B.V. All rights reserved.
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