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论文题目: Gprc5a-deficiency confers susceptibility to endotoxin-induced acute lung injury via NF-kappa B pathway
英文论文题目: Gprc5a-deficiency confers susceptibility to endotoxin-induced acute lung injury via NF-kappa B pathway
第一作者: Liao, YL; Song, HY; Xu, DL; Jiao, HK; Yao, F; Liu, JY; Wu, YD; Zhong, SS; Yin, HJ; Liu, SL; Wang, XF; Guo, WZ; Sun, BB; Han, BH; Chin, YE; Deng, J
英文第一作者: Liao, YL; Song, HY; Xu, DL; Jiao, HK; Yao, F; Liu, JY; Wu, YD; Zhong, SS; Yin, HJ; Liu, SL; Wang, XF; Guo, WZ; Sun, BB; Han, BH; Chin, YE; Deng, J
联系作者: Deng, J (reprint author), Shanghai Jiao Tong Univ, Sch Med, Key Lab Cell Differentiat & Apoptosis, Dept Pathophysiol,Chinese Minist Educ, Shanghai 200030, Peoples R China.
英文联系作者: Deng, J (reprint author), Shanghai Jiao Tong Univ, Sch Med, Key Lab Cell Differentiat & Apoptosis, Dept Pathophysiol,Chinese Minist Educ, Shanghai 200030, Peoples R China.
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发表年度: 2015
卷: 14
期: 9
页码: 1403-1412
摘要: Susceptibility to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) varies greatly among patients in sepsis/septic shock. The genetic and biochemical reasons for the difference are not fully understood. G protein coupled receptor family C group 5 member A (GPRC5A), a retinoic acid target gene, is predominately expressed in the bronchioalveolar epithelium of lung. We hypothesized that Gprc5a is important in controlling the susceptibility to ALI or ARDS. In this study, we examined the susceptibility of wild-type and Gprc5a-knockout (ko) mice to induced ALI. Administration of endotoxin LPS induced an increased pulmonary edema and injury in Gprc5a-ko mice, compared to wild-type counterparts. Consistently, LPS administration induced higher levels of inflammatory cytokines (IL-1 beta and TNF alpha) and chemokine (KC) in Gprc5a-ko mouse lungs than in wild-type. The enhanced pulmonary inflammatory responses were associated with dysregulated NF-kappa B signaling in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs. Importantly, selective inhibition of NF-kappa B through expression of the super-repressor I kappa B alpha in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs alleviated the LPS-induced pulmonary injury, and inflammatory response. Thus, Gprc5a is critical for lung homeostasis, and Gprc5a deficiency confers the susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-kappa B signaling in bronchioalveolar epithelium of lung.
英文摘要: Susceptibility to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) varies greatly among patients in sepsis/septic shock. The genetic and biochemical reasons for the difference are not fully understood. G protein coupled receptor family C group 5 member A (GPRC5A), a retinoic acid target gene, is predominately expressed in the bronchioalveolar epithelium of lung. We hypothesized that Gprc5a is important in controlling the susceptibility to ALI or ARDS. In this study, we examined the susceptibility of wild-type and Gprc5a-knockout (ko) mice to induced ALI. Administration of endotoxin LPS induced an increased pulmonary edema and injury in Gprc5a-ko mice, compared to wild-type counterparts. Consistently, LPS administration induced higher levels of inflammatory cytokines (IL-1 beta and TNF alpha) and chemokine (KC) in Gprc5a-ko mouse lungs than in wild-type. The enhanced pulmonary inflammatory responses were associated with dysregulated NF-kappa B signaling in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs. Importantly, selective inhibition of NF-kappa B through expression of the super-repressor I kappa B alpha in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs alleviated the LPS-induced pulmonary injury, and inflammatory response. Thus, Gprc5a is critical for lung homeostasis, and Gprc5a deficiency confers the susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-kappa B signaling in bronchioalveolar epithelium of lung.
刊物名称: CELL CYCLE
英文刊物名称: CELL CYCLE
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 4.565
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论文类别: Article
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