A feedback loop in PPARγ–adenosine A2A receptor signaling inhibits inflammation and attenuates lung damages in a mouse model of LPS-induced acute lung injury - He, Xie; Hu, Jian-Lin; Li, Jun; Zhao, Li; Zhang, Yan; Zeng, Yi-Jun; Dai, Shuang-Shuang; He, Feng-Tian (Cellular signalling, 2013)
Keywords: A2AR; Acute Lung Injury - genetics; Acute Lung Injury - immunology; Acute Lung Injury - pathology; Acute Lung Injury - prevention & control; adenosine; Adenosine A2 Receptor Agonists - therapeutic use; agonists; ALI; animal models; Animals; anti-inflammatory activity; binding proteins; blood gases; cAMP-dependent protein kinase; Cell Line; Cells, Cultured; cytokines; Cytokines - immunology; edema; gas exchange; gene expression regulation; genes; Inflammation; Inflammation - genetics; Inflammation - immunology; Inflammation - pathology; Inflammation - prevention & control; Lipopolysaccharides; Lung - drug effects; Lung - immunology; Lung - pathology; lung function; macrophages; Macrophages - drug effects; Macrophages - immunology; messenger RNA; Mice; neutrophils; PPAR gamma - agonists; PPAR gamma - genetics; PPAR gamma - immunology; PPARγ; promoter regions; Receptor, Adenosine A2A - genetics; Receptor, Adenosine A2A - immunology; RNA, Messenger - genetics; Signal Transduction; tissues; Transcriptional Activation; Up-Regulation; Inflammation; A2AR; PPARγ; ALI