Significant Elevation of Serum Human Hepatocyte Growth Factor Levels in Patients with Acute Pancreatitis

Ueda, Takashi; Takeyama, Yoshifumi; Toyokawa, Akihiro; Kishida, Shosei; Yamamoto, Masahiro; Saitoh, Yoichi

doi:10.1097/00006676-199601000-00010

Cited by 47 publications

(29 citation statements)

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“…8) HGF elevation occurs postoperatively due to surgical injury near the cancer lesion or in normal tissues. [11][12][13] Blood HGF concentration increases in patients who have Fig. 4 Comparison of disease-free interval between high HGF patients and low HGF patients after lung surgery.…”

Section: Survival Analysismentioning

confidence: 99%

“…HGF: hepatocyte growth factor undergone major surgery or inflammation 10,12) or patients suffering from Systemic Inflammatory Reaction Syndrome 11) or pancreatitis. 13) According to in vivo models, tumor metastasis to the lung may be enhanced by normal tissue injury. 25) Tumor cells circulating in the peripheral blood were detected using several techniques: immunohistochemistry, RT-PCR, and flow cytometry.…”

Section: Survival Analysismentioning

confidence: 99%

“…7) Additionally, some investigators have reported that HGF production is caused by several types of tissue damage. [9][10][11][12][13] Surgical injury itself may be a trigger for cytokine production or HGF conversion by HGF activator. Several in vitro studies have revealed that HGF activation results from elevated IL-6 expression.…”

Section: Introductionmentioning

confidence: 99%

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Plasma Hepatocyte Growth Factor Elevation May Be Associated with Early Metastatic Disease in Primary Lung Cancer Patients

Hosoda

Hayashi

Tukada

et al. 2012

Ann Thorac Cardiovasc Surg

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Purpose: Hepatocyte growth factor (HGF), a ligand of the c-met proto-oncogene, exhibits activating effects on human lung cancer both in vitro and in vivo. However, few studies have reported the correlations between concentration changes of blood HGF and postsurgical prognosis. Methods: We evaluated whether surgery-related blood HGF elevation has prognostic significance in patients with surgically resected non-small cell lung cancer. We examined blood HGF concentration, c-met expression, and postoperative prognosis of 25 cases of primary resected, non-small cell lung cancer. Results: We divided the patients into 2 groups according to receiver operating characteristics curve analysis using 7.2 ng/mL as the cut-off value of blood HGF concentration. Survival curve analysis revealed that patients with a high level of HGF (over the cutoff value) exhibited a poor prognosis of metastatic disease, compared to those in the low-level group after curative surgery (log rank test, P = 0.020; Wilcoxon test, P = 0.016). Conclusion: Elevation of HGF in plasma may be an important prognostic factor for early metastatic disease in patients with primary lung cancer. Moreover, inhibition of HGF elevation may have therapeutic effects on early distant metastasis of lung cancer.

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Section: Survival Analysismentioning

confidence: 99%

Section: Survival Analysismentioning

confidence: 99%

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Plasma Hepatocyte Growth Factor Elevation May Be Associated with Early Metastatic Disease in Primary Lung Cancer Patients

Hosoda

Hayashi

Tukada

et al. 2012

Ann Thorac Cardiovasc Surg

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“…In vivo, HGF is important for the development of the placenta, liver, limbs, and kidney (6,28,67,71,72,82,87) and induces morphogenesis of blood vessels (9,22,47,70). In addition, both HGF and the c-met protooncogene (c-met) (31, 86), a tyrosine kinase receptor (11,19,51,54) to which HGF binds with high affinity (25,32), are regulated in response to organ injury and stimulate epithelial morphogenesis that contributes to tissue repair and regeneration in liver, kidney, lung, gastric mucosa, and muscle (12,38,40,66,81,88). In vitro, many of the pleiotropic effects of HGF can be modeled and show a dependence on both the target cell type and environmental context: paracrine actions of HGF increase hepatocyte mitogenesis (20,41,49,50,90), inhibit growth of tumor cells (69, 78), activate motogenesis and invasiveness of epithelial and endothelial cells (9,18,63,64,70,75,84,85), stimulate wound repair (53), and induce morphogenesis of either epithelial tubes or pseudostratified layers from polarized epithelial monolayers (4,42,43,56,73)…”

mentioning

confidence: 99%

Hepatocyte growth factor induces MDCK cell morphogenesis without causing loss of tight junction functional integrity

Pollack¹,

Apodaca²,

Mostov³

2004

American Journal of Physiology-Cell Physiology

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Hepatocyte growth factor (HGF) induces mitogenesis, motogenesis, and tubulogenesis of cultured Madin-Darby canine kidney (MDCK) epithelial cells. We report that in addition to these effects HGF stimulates morphogenesis of tight, polarized MDCK cell monolayers into pseudostratified layers without loss of tight junction (TJ) functional integrity. We tested TJ functional integrity during formation of pseudostratified layers. In response to HGF, the TJ marker ZO-1 remained in morphologically complete rings and functional barriers to paracellular diffusion of ruthenium red were maintained in pseudostratified layers. Transepithelial resistance (TER) increased transiently two-to threefold during the morphogenetic transition from monolayers to pseudostratified layers and then declined to baseline levels once pseudostratified layers were formed. In MDCK cells expressing the trk/met chimera, both HGF and NGF at concentrations of 2.5 ng/ml induced scattering. However, 2.5 ng/ml HGF did not affect TER. The peak effect of HGF on TER was at a concentration of 100 ng/ml. In contrast, NGF at concentrations as high as 25 g/ml had no effect on TER or pseudostratified layer morphogenesis of trk/met-expressing cultures. These results suggest that altered presentation of the stimulus, such as through HGF interaction with low-affinity sites, may change the downstream signaling response. In addition, our results demonstrate that HGF stimulates pseudostratified layer morphogenesis while inducing an increase in TER and maintaining the overall tightness of the epithelial layer. Stimulation of epithelial cell movements by HGF without loss of functional TJs may be important for maintaining epithelial integrity during morphogenetic events such as formation of pseudostratified epithelia, organ regeneration, and tissue repair. c-met protooncogene; transepithelial resistance; Madin-Darby canine kidney cell MORPHOGENETIC CELL REARRANGEMENTS are stimulated by hepatocyte growth factor (HGF), a fibroblast-derived growth factor (77) that has paracrine actions on a variety of cell types. In vivo, HGF is important for the development of the placenta, liver, limbs, and kidney (6,28,67,71,72,82,87) and induces morphogenesis of blood vessels (9,22,47,70). In addition, both HGF and the c-met protooncogene (c-met) (31, 86), a tyrosine kinase receptor (11,19,51,54) to which HGF binds with high affinity (25,32), are regulated in response to organ injury and stimulate epithelial morphogenesis that contributes to tissue repair and regeneration in liver, kidney, lung, gastric mucosa, and muscle (12,38,40,66,81,88). In vitro, many of the pleiotropic effects of HGF can be modeled and show a dependence on both the target cell type and environmental context: paracrine actions of HGF increase hepatocyte mitogenesis (20,41,49,50,90), inhibit growth of tumor cells (69, 78), activate motogenesis and invasiveness of epithelial and endothelial cells (9,18,63,64,70,75,84,85), stimulate wound repair (53), and induce morphogenesis of either epithelial tubes or pseudostrati...

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“…The involvement of COX-2 in IP effects on the pancreas is similar to that observed after treatment with HGF. Serum concentration of HGF is increased in patients with acute pancreatitis, and the HGF level reflects the clinical severity of pancreatitis and organ dysfunction [33,34] . Also experimental studies have shown the increase in plasma HGF level and tissue HGF overexpression in acute pancreatitis [35,36] .…”

Section: Effect Of Ischemic Preconditioning and Cerulein-induced Pancmentioning

confidence: 99%

Ischemic preconditioning inhibits development of edematous cerulein-induced pancreatitis: Involvement of cyclooxygenases and heat shock protein 70

Warzecha

Dembiński²,

Ceranowicz³

et al. 2005

WJG

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Abstract Abstract Abstract AIM: To determine whether ischemic preconditioning (IP) affects the development of edematous cerulein-induced pancreatitis and to assess the role of cyclooxygenase-1 (COX-1), COX-2, and heat shock protein 70 (HSP 70) in this process. METHODS:In male Wistar rats, IP was performed by clamping of celiac artery (twice for 5 min at 5-min intervals). Thirty minutes after IP or sham operation, acute pancreatitis was induced by cerulein. Activity of COX-1 or COX-2 was inhibited by resveratrol or rofecoxib, respectively (10 mg/kg). RESULTS:IP significantly reduced pancreatic damage in cerulein-induced pancreatitis as demonstrated by the improvement of pancreas histology, reduction in serum lipase and poly-C ribonuclease activity, and serum concentration of pro-inflammatory interleukin (IL)-1β. Also, IP attenuated the pancreatitis-evoked fall in pancreatic blood flow and pancreatic DNA synthesis. Serum level of anti-inflammatory IL-10 was not affected by IP. Cerulein-induced pancreatitis and IP increased the content of HSP 70 in the pancreas. Maximal increase in HSP 70 was observed when IP was combined with cerulein-induced pancreatitis. Inhibition of COXs, especially COX-2, reduced the protective effect of IP in edematous pancreatitis. CONCLUSION:Our results indicate that IP reduces pancreatic damage in cerulein-induced pancreatitis and this effect, at least in part, depends on the activity of COXs and pancreatic production of HSP 70.

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Significant Elevation of Serum Human Hepatocyte Growth Factor Levels in Patients with Acute Pancreatitis

Cited by 47 publications

References 0 publications

Plasma Hepatocyte Growth Factor Elevation May Be Associated with Early Metastatic Disease in Primary Lung Cancer Patients

Plasma Hepatocyte Growth Factor Elevation May Be Associated with Early Metastatic Disease in Primary Lung Cancer Patients

Hepatocyte growth factor induces MDCK cell morphogenesis without causing loss of tight junction functional integrity

Ischemic preconditioning inhibits development of edematous cerulein-induced pancreatitis: Involvement of cyclooxygenases and heat shock protein 70

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