Gastroenterology Research and Practice / 2012 / Article / Tab 1 / Review Article
Improvement of Sepsis by Hepatocyte Growth Factor, an Anti-Inflammatory Regulator: Emerging Insights and Therapeutic Potential Table 1 Biological effects of HGF on target cells, involved in sepsis-related MOF.
Target cells Effect Involved mechanism References Epithelial cells Mitogenesis Grab2-MAPK [13 ] Migration Gab1-PI3K [13 ] Morphogen Gab1-PI3K [13 ] Anti-apoptosis Bcl-xL induction [15 , 40 ] Vascular cells Endothelium Mitogenesis MAP-kinase [10 ] Anti-inflammation Anti-NF-κ B [32 , 41 –43 ] Anti-apoptosis Bcl-2 upregulation [10 ] Anti-coagulation TM preservation [44 , 45 ] Pericytes Anti-proliferation Anti-MAPK [10 , 15 ] Immune cells Macrophages Anti-cytokine storm HO-1 upregulation [28 , 29 ] Anti-NFκ B activation GSK3β de-phosphorylation [46 ] DC Tolerogenic effects TH1 ≪ TH2 balance [10 , 30 ] Eosinophils Anti-inflammation Inhibition of eosinophilic toxin release [10 ] T-lymphocytes Anti-proliferation IFN-γ downregulation [10 ]
Epithelial cells include hepatocytes, renal tubular cells, and alveolar and bronchial epithelium. TM: thrombomodulin; DC: dendritic cells; GSK3β : glycogen synthase kinase-3β . For abbreviations see text or original references.