Stem Cell Factor Levels Do Increase in Patients Subsequent to Hepatectomy With the Extent of Parenchymal Loss

Krieg, Andreas; Esch, Jan Schulte Am; Schmelzle, Moritz; Tustas, R.; Elkarmi, Ali; Hosch, Stefan B.; Knoefel, Wolfram Trudo

doi:10.1016/j.transproceed.2006.10.111

Cited by 10 publications

(11 citation statements)

References 10 publications

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“…Increased serum levels of HGF have previously been observed after right hepatectomy for living‐related donation in healthy individuals and are known to be associated with homing of CD34 + stem cells . Our findings of significant increase in HGF within the first 24 h following resection further supports our previous report of increased HGF expression . Similar to HGF, both SDF‐1 and IGF‐1, were also expressed within the liver in the first 3–6 h post‐resection.…”

Section: Discussionsupporting

confidence: 91%

“…It is well established that the damaged liver releases chemokines and possible chemotactants, such as stroma‐derived factor‐1 (SDF‐1), stem cell factor (SCF), hepatocellular growth factor (HGF), insulin‐like growth factor (IGF‐1) and others, to participate in the concert of inflammatory cell homing from extrahepatic sources to the liver in rodents and humans . HGF seems to promote murine mobilization and SCF‐dependent recruitment of haematopoietic CD34 + cells from BM into the liver .…”

mentioning

confidence: 99%

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HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection

Lehwald

Duhme

Wildner

et al. 2013

Liver International

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection

Lehwald

Duhme

Wildner

et al. 2013

Liver International

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“…This process involves, on the one hand, cells permanently located in the liver and cells of the hematopoietic compartment and, on the other hand, a variety of humoral factors, including particularly stromal cell-derived factor (SDF-1), matrix metalloproteinases (MMPs), hepatocyte growth factor (HGF) and the interleukin-8 (IL-8) [18].…”

Section: Discussionmentioning

confidence: 99%

Reduced Mobilisation of Hematopoietic Stem Cells After Hepatic Resection for Malignant Liver Disease

Menegazzo¹,

Bagatella

Marson

et al. 2008

Pathol. Oncol. Res.

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Recent studies have demonstrated that hematopoietic stem cells (HSCs) can mobilize following liver resection, thus contributing to the repair of hepatic damage. Aim of this study has been to determine whether the nature of the hepatic lesion (benign vs. malignant disease) can give rise to a different degree of mobilisation of HSCs. Two groups of patients were selected: the first included seven patients undergoing hepatic resection (five major and two minor) for a benign liver disease (focal nodular hyperplasia, hemangioma cavernosa, angioma, biliary adenofibroma) and the second included seven patients undergoing hepatic resection (five major and two minor) for a malignant (either primary or secondary) liver disease. White blood cell count and CD34+ (percentage and total number) at time T(0) (basal value before surgery) and at time T(1) (value on the sixth-eighth day after surgery) have been evaluated by standard methods. In the group undergoing hepatic resection for a benign liver disease, a significant increase of CD34+ cells, both in percentage (0.082 +/- 0.043 vs. 0.048 +/- 0,026, p = 0.041) and in absolute number (8.14 +/- 5.95 vs. 3.26 +/- 2.63, p = 0.018) have been documented, as opposed to the group of patients affected with a malignant liver disease, where no significant variation has been observed (CD34+ %: 0.044 +/- 0.033 vs. 0.041 +/- 0.031, p: n.s.; CD34+ total number: 3.52 +/- 2.56 vs. 2.27 +/- 2.01, p = n.s.) These results show a different bone marrow response to the surgical liver resection depending on the nature of the lesion, thus emphasizing a reduced mobilisation of HSCs in the malignant diseases. Since it has been documented that the type of the hepatic lesion can induce a different regenerative response, it has to be explained how the neoplastic lesions can negatively influence the mobilization of HSCs. It can be hypothesized that a variety of humoral factors, including stromal cell-derived factor, matrix metalloproteinases, hepatocyte growth factor and interleukin-8 can influence the process of mobilization of HSCs after liver resection surgery. These substances are also involved in the mechanisms of development and metastasising of many tumours. It is probably in this context that a reason may be found for the different mobilisation of hematopoietic stem cells, depending on the nature of the hepatic lesion treated, that was encountered in this study.

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“…16,43 Earlier studies showed, in murine models of liver injury and in patients with hepatectomy, that SCF levels do increase with the extent of parenchymal loss, whereas patients with fulminant hepatic failure had significantly lower levels of SCF, emphasizing the role of SCF and c-Kit in liver repair. 14,44 Recent studies have documented that SCF is produced and released in response to hepatic resection, inducing hepatocyte proliferation. Proliferative effects on hepatocytes could be shown both in vitro and in vivo after partial hepatectomy, whereby IL-6 and TNF-a were supposed to induce hepatocyte production of SCF.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 Besides regulating the hemopoietic stem cell proliferation, SCF has been implicated in inflammatory diseases, tissue remodeling--including fibrosis--and in liver regeneration after liver injury, suggesting that it may serve as a protective factor in tissues that could be susceptible to environmental-toxic injury. [14][15][16][17][18] However, further studies indicate that, in addition to its physiological functions, SCF plays a critical role in carcinogenesis and is co-expressed with its receptor, c-Kit, in various tumors, implying the possible presence of an autocrine and/or a paracrine loop. [19][20][21][22][23] In this manner, it seems that several cell populations can express and quickly release SCF upon cellular assault or inflammation.…”

mentioning

confidence: 99%

Expression of stem cell factor and its receptor c-Kit during the development of intrahepatic cholangiocarcinoma

Mansuroglu

Ramadori

Dudás

et al. 2009

Laboratory Investigation

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Stem cell factor (SCF) and its receptor, c-Kit, constitute an important signal transduction system with proliferative and anti-apoptotic functions. Besides regulating hemopoietic stem cell proliferation and liver regeneration, it has been implicated in the regulation of human malignancies. However, the cellular expression of the SCF-c-Kit gene system in the liver during cholangiocarcinogenesis has not been studied to date. The protein-and mRNA-expression levels of SCF and c-Kit genes were examined in normal rat liver, in isolated normal rat liver cells and in a thioacetamide-induced rat model of intrahepatic cholangiocarcinoma (CC). Immunohistochemical analysis of the normal liver showed that SCF is expressed in the wall of the hepatic artery and in some cells, which were located along the sinusoids, although it was absent from hepatocytes and biliary epithelial cells. The mRNA analysis of isolated normal liver cell populations revealed a co-expression of SCF-and c-Kit-mRNA in sinusoidal endothelial cells and in Kupffer cells, whereas passaged and cultured liver myofibroblasts (MFs) expressed only SCF. Low levels of the SCF-and c-Kit-mRNA expression could be detected in isolated hepatocytes of the normal liver. Immunohistochemical analysis of the CC tissue showed SCF positivity in proliferating biliary cells (CK-19 þ ), in macrophages (ED-1 þ ) and in MFs (a-smooth-muscle-actin, a-SMA þ ) of the tumoral microenvironment. c-Kit-positivity could be detected on hepatocytes of the regenerating nodules and on the proliferating bile ducts of CC. Compared with the normal liver tissue, SCF-mRNA from the CC tissue was upregulated up to 20-fold, whereas c-Kit-mRNA was upregulated up to fivefold. These data indicate that several cell populations may become able to express SCF and/or c-Kit during cholangiocarcinogenesis. Therefore, the SCF-c-Kit system may contribute to tumor development, for instance, by inducing proliferation of hepatocytes and of biliary cells and by acting as a surviving factor for CC cells.

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Stem Cell Factor Levels Do Increase in Patients Subsequent to Hepatectomy With the Extent of Parenchymal Loss

Cited by 10 publications

References 10 publications

HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection

HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection

Reduced Mobilisation of Hematopoietic Stem Cells After Hepatic Resection for Malignant Liver Disease

Expression of stem cell factor and its receptor c-Kit during the development of intrahepatic cholangiocarcinoma

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Stem Cell Factor Levels Do Increase in Patients Subsequent to Hepatectomy With the Extent of Parenchymal Loss

Cited by 10 publications

References 10 publications

HGF and SDF‐1‐mediated mobilization of CD133+BMSC for hepatic regeneration following extensive liver resection

HGF and SDF‐1‐mediated mobilization of CD133+BMSC for hepatic regeneration following extensive liver resection

Reduced Mobilisation of Hematopoietic Stem Cells After Hepatic Resection for Malignant Liver Disease

Expression of stem cell factor and its receptor c-Kit during the development of intrahepatic cholangiocarcinoma

Contact Info

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HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection

HGF and SDF‐1‐mediated mobilization of CD133⁺BMSC for hepatic regeneration following extensive liver resection