Early gene expression of hepatocyte growth factor in mononuclear phagocytes of rat liver after administration of carbon tetrachloride

Armbrust, Thomas; Batusic, Danko; Xia, Li-Qun; Ramadori, Giuliano

doi:10.1034/j.1600-0676.2002.01731.x

Cited by 25 publications

(24 citation statements)

References 34 publications

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“…MMP-2 and MMP-9 can also increase recruitment of CD34 + cells via other pathways, such as shedding of membrane-bound SCF and autocrine secretion of these enzymes by CD34 + progenitors in response to SDF-1 stimulation (42,43). Acute liver injury triggers the expression of other factors, such as the pleiotropic cytokine HGF (31). We demonstrate for the first time that HGF also induces cytoskeleton rearrangement and increases the motility of and potentiates the response of immature CD34 + cells to SDF-1 signaling by inducing CXCR4 upregulation and synergizing with SCF.…”

Section: Discussionmentioning

confidence: 99%

“…HGF is upregulated in the injured liver following CCl 4 administration (31), and the addition of human HGF increases the levels of human albumin-producing cells in CCl 4 -injured livers of engrafted immune-deficient murine chimeras (10). We therefore hypothesized that HGF may also participate in the regulation of human CD34 + cell migration and recruitment to the injured liver.…”

Section: Stress-induced Mmp-2/mmp-9 Expression Recruits Cxcr4 + Hematmentioning

confidence: 99%

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HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver

Kollet¹,

Shivtiel²,

Chen³

et al. 2003

J. Clin. Invest.

547

348

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Hematopoietic stem cells rarely contribute to hepatic regeneration, however, the mechanisms governing their homing to the liver, which is a crucial first step, are poorly understood. The chemokine stromal cell-derived factor-1 (SDF-1), which attracts human and murine progenitors, is expressed by liver bile duct epithelium. Neutralization of the SDF-1 receptor CXCR4 abolished homing and engraftment of the murine liver by human CD34 + hematopoietic progenitors, while local injection of human SDF-1 increased their homing. Engrafted human cells were localized in clusters surrounding the bile ducts, in close proximity to SDF-1-expressing epithelial cells, and differentiated into albumin-producing cells. Irradiation or inflammation increased SDF-1 levels and hepatic injury induced MMP-9 activity, leading to both increased CXCR4 expression and SDF-1-mediated recruitment of hematopoietic progenitors to the liver. Unexpectedly, HGF, which is increased following liver injury, promoted protrusion formation, CXCR4 upregulation, and SDF-1-mediated directional migration by human CD34 + progenitors, and synergized with stem cell factor. Thus, stress-induced signals, such as increased expression of SDF-1, MMP-9, and HGF, recruit human CD34 + progenitors with hematopoietic and/or hepatic-like potential to the liver of NOD/SCID mice. Our results suggest the potential of hematopoietic CD34 + /CXCR4 + cells to respond to stress signals from nonhematopoietic injured organs as an important mechanism for tissue targeting and repair.

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Section: Discussionmentioning

confidence: 99%

Section: Stress-induced Mmp-2/mmp-9 Expression Recruits Cxcr4 + Hematmentioning

confidence: 99%

HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver

Kollet¹,

Shivtiel²,

Chen³

et al. 2003

J. Clin. Invest.

547

348

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show abstract

“…32, No. 5, 2004 ALCOHOL AND LIVER REGENERATION 575 MAPK has been documented in both partial hepatectomy and toxicant-induced liver injury models (Taub, 1996;Saso et al, 1997;Apte et al, 2002;Armbrust et al, 2002;Diehl, 2002b;Fausto and Campbell, 2003). Based on these reports, we selected JNK pathway (NF-κB) and MAPK pathway (ERK1/2 and p38).…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte Proliferation is the Possible Mechanism for the Transient Decrease in Liver Injury During Steatosis Stage of Alcoholic Liver Disease

Apte¹,

McRee²,

Ramaiah³

2004

Toxicol Pathol

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Steatosis is a frequent pathologic stage in alcoholic liver disease (ALD). Although the mechanisms for increased susceptibility of steatotic liver to injury have been postulated, the ability of these hepatocytes to proliferate and withstand injury is unknown. There are conflicting reports on the status of hepatocyte regeneration following chronic alcohol ingestion. Hence, the objective of this study was to investigate the temporal dynamics between the pattern of liver injury and hepatocyte proliferation during the steatosis stage of ALD. Alcoholic steatosis was induced in male Sprague-Dawley rats by feeding an ethanol (EtOH)-containing Lieber-DeCarli liquid diet for a period of 5 weeks. Microvesicular steatosis was evident in H&E sections by three weeks in the EtOH-treated rats, which further developed into panlobular macrovesicular steatosis by 5 weeks. Plasma transaminase activities indicated progressive increase in liver injury peaking at 3 weeks with significant but mild decrease at 4 and 5 weeks. CYP2E1 protein and activity was significantly increased in EtOH-fed rats as measured by Western blot and pNP hydroxylation assay. PCNA analysis of liver sections indicated that EtOH-treated rats had a significantly higher number of cells in S phase of cell division at weeks 1 (3.20 ± 0.19), 2 (7.03 ± 0.92), and 3 (4.23 ± 1.41) when compared to controls (1.5 ± 0.22). NF-κB DNA binding and Cyclin D1 proteins increased significantly in the EtOH-treated rats corresponding with enhanced hepatic proliferation. These data suggest the transient decline in liver injury during alcoholic steatosis is due to enhanced NF-κB-dependent hepatocyte proliferation.

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“…Nonetheless, KC function was found to be essential for hepatocellular proliferation and crucial in liver regeneration (Malik et al, 2002;Bilzer et al, 2006;Abshagen et al, 2007). In particular, hepatocyte growth factor as well as the cytokines IL-6 (Aldeguer et al, 2002) and TNF-␣ (Kirillova et al, 1999;Abshagen et al, 2007) provided by Kupffer cells and endothelial cells stimulate hepatocyte proliferation by triggering hepatocytic DNA replication via NF-〉 (Seto et al, 1998;Armbrust et al, 2002;Bruun et al, 2002;Lalani et al, 2005;Bastard et al, 2006;Wang et al, 2006a;Simons et al, 2007). In addition, Kupffer cells seem to be involved in maintenance of adequate perfusion during liver cell proliferation-a function that could be related to Kupffer cell-derived cytokines or Kupffer cell-mediated effects on nitric oxide metabolism, which apparently plays an important role in hepatic microcirculation, particularly after liver injury (Rolfe et al, 1997;West et al, 1999;Holden et al, 2000;Meijer et al, 2000, Abshagen et al, 2008Palmes et al, 2005;Schuett et al, 2007).…”

Section: Cross-talk Of Hepatocytes With Stellate Cells Fibroblasts mentioning

confidence: 99%

Molecular Mechanisms and Therapeutic Targets in Steatosis and Steatohepatitis

Anderson

Borlak²

2008

Pharmacological Reviews

342

255

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Early gene expression of hepatocyte growth factor in mononuclear phagocytes of rat liver after administration of carbon tetrachloride

Cited by 25 publications

References 34 publications

HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver

HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver

Hepatocyte Proliferation is the Possible Mechanism for the Transient Decrease in Liver Injury During Steatosis Stage of Alcoholic Liver Disease

Molecular Mechanisms and Therapeutic Targets in Steatosis and Steatohepatitis

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