scholarly journals Anti-Inflammatory Effect of Hepatocyte Growth Factor in Chronic Kidney Disease: Targeting the Inflamed Vascular Endothelium

2006 ◽  
Vol 17 (9) ◽  
pp. 2464-2473 ◽  
Author(s):  
Rujun Gong ◽  
Abdalla Rifai ◽  
Lance D. Dworkin
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Hepatocyte Growth Factor ◽  
Vascular Endothelium ◽  
Anti Inflammatory ◽  
Hepatocyte Growth ◽  
Inflammatory Effect

Piceatannol increases the expression of hepatocyte growth factor and IL-10 thereby protecting hepatocytes in thioacetamide-induced liver fibrosis

2016 ◽  
Vol 94 (7) ◽  
pp. 779-787 ◽  
Author(s):  
Hazem Abd-Elgawad ◽  
Nashwa Abu-Elsaad ◽  
Amr El-Karef ◽  
Tarek Ibrahim
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Liver Function ◽  
Hepatocyte Growth Factor ◽  
Transforming Growth Factor ◽  
Histopathological Examination ◽  
Smooth Muscle Actin ◽  
Interleukin 10 ◽  
Hepatocyte Growth ◽  
Inflammatory Effect

Piceatannol is a polyphenolic analog of resveratrol that selectively inhibits the non-receptor tyrosine kinase-Syk. This study investigates the potential ability of piceatannol to attenuate liver fibrosis and protect hepatocytes from injury. Thioacetamide was injected in adult male mice (100 mg/kg, i.p., 3 times/week) for 8 weeks. Piceatannol (1 or 5 mg/kg per day) was administered by oral gavage during the last 4 weeks. Liver function biomarkers, tissue malondialdehyde (MDA), cytokeratin-18 (CK18), hepatocyte growth factor (HGF), and interleukin-10 (IL-10) were measured. Necroinflammation, fibrosis, expression of transforming growth factor (TGF)-β1, and α-smooth muscle actin (SMA) were scored by histopathological examination and immunohistochemistry. Obtained results showed ability of piceatannol (1 mg/kg) to restore liver function and reduce inflammation. It significantly (p < 0.001) reduced MDA, CK18, TGF-β1, and α-SMA expression, and increased HGF and IL-10. It can be concluded that piceatannol at low dose can inhibit TGF-β1 induced hepatocytes apoptosis and exerts an anti-inflammatory effect attenuating fibrosis progression.

scholarly journals Hepatocyte Growth Factor Exerts Its Anti-Inflammatory Action by Disrupting Nuclear Factor-κB Signaling

2008 ◽  
Vol 173 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Myrto Giannopoulou ◽  
Chunsun Dai ◽  
Xiaoyue Tan ◽  
Xiaoyan Wen ◽  
George K. Michalopoulos ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Anti Inflammatory ◽  
Hepatocyte Growth ◽  
Inflammatory Action

Up-Regulation of Anti-Inflammatory, STAT3-Activating Hepatocyte Growth Factor and Interleukin-11 In Polycythemia Vera Is Independent of JAK2V617F and Contributes to the Growth of Clonal Erythroblasts

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 796-796
Author(s):  
Marjorie Boissinot ◽  
Cedric Cleyrat ◽  
Mathias Vilaine ◽  
Yannick Jacques ◽  
Isabelle Corre ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Polycythemia Vera ◽  
Neutralizing Antibodies ◽  
Conflicts Of Interest ◽  
Mrna Levels ◽  
Hel Cells ◽  
Anti Inflammatory ◽  
Hepatocyte Growth ◽  
Interleukin 11

Abstract Abstract 796 Context: The V617F activating mutation of JAK2, JAK2V617F, characterizes Polycythemia vera (PV). However, expression of JAK2V617F does not always result in clone expansion, implying that additional events are required for the growth of JAK2-mutated progenitors and development of the PV phenotype. In the present study, we provide evidence that anti-inflammatory cytokines are required for the growth of JAK2V617F-mutated erythroid progenitors. Methods: We searched for cytokines over-expressed in PV using cytokine antibody arrays and ELISAs for analyses of serum and bone marrow (BM) plasma, and quantitative RT-PCRs for analyses of cells purified from PV patients and controls. Transient transfection of JAK2V617F and invalidation of JAK2V617F with siRNA were used to study the effect of JAK2V617F on cytokine expression. Results: We found that PV patients over-expressed anti-inflammatory hepatocyte growth factor (HGF) and interleukin-11 (IL-11), BM stromal cells (BMSC) and erythroblasts being the main producers. HGF induced the production of IL-11 and both cytokines activate the STAT3 pathway. We used neutralizing antibodies specific for IL-11 or c-MET, the HGF receptor, to block autocrine/paracrine cytokine stimulation of erythroblasts in in vitro cultures. The growth of JAK2V617F-mutated PV erythroblasts and HEL cells was inhibited by at least 40%, indicating that JAK2V617F-mutated cells depend on HGF and IL-11 for their growth. Consistent with activation of HGF/IL-11 pathways, mRNA levels of gp130 (the receptor chain responsible for signalling common to cytokines of the IL-11/IL-6 family) and STAT3 were significantly elevated in PV erythroblasts. Moreover, mRNA levels of c-MET, HGF and IL-11 were correlated, a logical finding as c-MET, HGF and IL-11 act in cascade. No correlation was found with JAK2V617F mRNA levels. To the opposite, we provide evidence that the up-regulation of HGF and IL-11 in PV is not a consequence of JAK2V617F: transient expression of JAK2V617F in BaF-3/Epo-R cells and invalidation of JAK2V617F in HEL cells using anti-JAK2 siRNA had no effect on HGF and IL-11 expression. Conclusion: Anti-inflammatory, STAT3-activating HGF and IL-11 are up-regulated in PV independently of JAK2V617F. Both cytokines contribute to the proliferation of JAK2V617F-mutated erythroblasts, suggesting that drugs blocking the HGF/IL-11 pathways, such as c-MET antagonists, could be of interest as an additional therapeutic option in PV. Marjorie Boissinot and Cedric Cleyrat contibuted equally. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Anti-inflammatory activities of hepatocyte growth factor in post-ischemic heart failure

2018 ◽  
Vol 39 (10) ◽  
pp. 1613-1621 ◽  
Author(s):  
Shu-ling Rong ◽  
Xiao-lin Wang ◽  
Yi-cheng Wang ◽  
Huan Wu ◽  
Xue-dong Zhou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Ischemic Heart ◽  
Ischemic Heart Failure ◽  
Anti Inflammatory ◽  
Hepatocyte Growth

Interaction of Hepatocyte Growth Factor and Non-Steroidal Anti-Inflammatory Drugs during Gastric Epithelial Wound Healing

Digestion ◽  
2003 ◽  
Vol 67 (3) ◽  
pp. 118-128 ◽  
Author(s):  
Peter Netzer ◽  
Fred Halter ◽  
Thomas Y. Ma ◽  
Neil Hoa ◽  
Nathan Nguyen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Epithelial Wound Healing ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Hepatocyte Growth
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