Cooperative Roles of Hepatocyte Growth Factor and Plasminogen Activator in Tubular Morphogenesis by Human Microvascular Endothelial Cells

Morimoto, Akio; Tada, Katsuhiro; Nakayama, Yoshifumi; Kohno, Kimitoshi; Naito, Seiji; Ono, Masahiro; Kuwano, Michihiko

doi:10.1111/j.1349-7006.1994.tb02886.x

Cited by 20 publications

(15 citation statements)

References 47 publications

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“…Simultaneous upregulation of two different proteolytic activities by HGF/SF in the same cell line is shown here for the first time. Induction of uPA by HGF/SF had already been reported in other cell lines [18][19][20], and linked to in vitro invasiveness and in vivo metastatic potential [13]. The presence of uPA activity on the cell surface might start a positive feedback loop, since it is known that HGF/SF is bound as an inactive single-chain form to the heparan sulfates of the extracellular matrix [21,22], whence it can be activated through limited proteolysis by uPA [23].…”

Section: Discussionmentioning

confidence: 99%

Influence of Hepatocyte Growth Factor/Scatter Factor on the Metastatic Phenotype of B16 Melanoma Cells

Rusciano¹,

Lin²,

Lorenzoni³

et al. 1998

Tumor Biol

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B16 melanoma cells selected in mice for liver-specific metastasis (B16-LS9) overexpress a constitutively active form of the hepatocyte growth factor/scatter factor receptor (HGF/SFr), the product of the c-met proto-oncogene. HGF/SF can affect both invasion and growth of receptive cells. In fact, we show that overexpression of c-met in B16-LS9 cells results in a higher inducibility of two different proteolytic activities (uPA and gelatinase), in correlation with a stronger invasive and motility response to HGF/SF treatment. However, HGF/SF treatment inhibits growth of B16 cells, which might appear in contradiction with the observation that c-met overexpression and constitutive activation seems to be required for efficient liver colonization. However, this apparent discrepancy is resolved by the finding that liver-derived, but not lung-derived factor(s), can efficiently rescue B16-LS9 cells from the growth inhibitory effects of HGF/SF, while not changing their motility response. Therefore, overexpression of c-met in B16-LS9 cells might give a specific advantage in liver colonization, because specifically at this site B16-LS9 cells can take full advantage of the positive effects exerted by HGF/SF stimulation on motility and invasion, while the negative effects on growth are counteracted by other paracrine factor(s).

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Section: Discussionmentioning

confidence: 99%

Influence of Hepatocyte Growth Factor/Scatter Factor on the Metastatic Phenotype of B16 Melanoma Cells

Rusciano¹,

Lin²,

Lorenzoni³

et al. 1998

Tumor Biol

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“…12 In vitro and in vivo angiogenesis assays have established HGF to be a powerful angiogenic factor. [18][19][20] Initially identified as a stimulator of hepatocyte growth in vitro, it has since then been characterized as a cytokine with mitogenic, motogenic, and morphogenic effects, involved in various normal developmental and homeostatic processes of the body. 21 HGF is produced mainly by mesenchymal cells, like fibroblasts and vascular smooth muscle cells.…”

Section: Introductionmentioning

confidence: 99%

Plasma hepatocyte growth factor is a prognostic factor in patients with acute myeloid leukemia but not in patients with myelodysplastic syndrome

et al. 2001

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Hepatocyte growth factor (HGF) is a potent angiogenic factor. The aim of our study was to evaluate plasma HGF levels and their prognostic significance in patients with newly diagnosed acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). The sandwich enzyme immunoassay technique was used to quantify HGF in stored samples obtained before treatment from patients with AML (59 patients) and MDS (42 patients) treated at The University of Texas MD Anderson Cancer Center. HGF levels were significantly higher in patients with AML or MDS than in healthy individuals (P Ͻ 0.0001). Higher HGF levels in both AML and MDS correlated significantly with white blood cell (P = 0.000001 for both groups) and monocyte counts (P = 0.0004 and 0.003, respectively), and with poor performance status (P = 0.03 and 0.001, respectively). Using Cox proportional hazard model and HGF levels as a continuous variable, plasma levels of HGF correlated with shorter survival of AML (P = 0.001), but not MDS (P = 0.34) patients. No significant correlation was observed between HGF levels and complete remission rate or duration. In the multivariate analysis HGF retained its significance as prognostic factor in AML (P = 0.02), along with age (P = 0.0005). Leukemia (2001) 15, 1165-1170.

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“…In our laboratory, we have isolated HOME cells which show cobblestone morphology on collagen-coated plates or collagen gel (Mawatari et al, 1989). We have observed that EGF/TGF-a can stimulate migration of HOME cells and induce tube formation in type I collagen gel (Mawatari et al, 1991;Matsuda et al, 1992;Morimoto et al, 1991Morimoto et al, , 1994Ono et al, 1992;Okamura et al, 1992;Sat0 et al, 1993a,b). In addition, we have reported that the stimulatory effect of EGF/TGF-a on tube formation by HOME cells in type I collagen gel is dependent on increased t-PA activity (Okamura et al, A.…”

Section: Effects Of Egf and Tgf-p On Home Cells Cultured On Collagen mentioning

confidence: 90%

“…inhibitors in the presence of anti-TGF-p antibody We reported previously that EGF/TGF-a-induced cell migration and tubulogenesis of HOME cells are closely coupled with expression of t-PA (Mawatari et al, 1991;Morimoto et al, 1991Morimoto et al, , 1994Okamura et al, 1992;Sat0 et al, 1993a,b). Tubulogenesis was assayed in type I collagen gel Ono et al, 1992;Sat0 et al, 1993a;Morimoto et al, 1994).…”

Section: Expression Of T-pa Collagenase and Theirmentioning

confidence: 93%

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Expression of tissue‐type plasminogen activator and its inhibitor couples with development of capillary network by human microvascular endothelial cells on matrigel

Ito

Ryuto

Ushiro

et al. 1995

Journal Cellular Physiology

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Human omental microvascular endothelial (HOME) cells seeded on Matrigel begin to migrate within 1 h, forming honeycomb-like structures and capillary-like networks within 18 h. Cross-sections of the capillary networks show them to be tube-like structures. Northern blot analysis showed that tissue-type plasminogen activator (t-PA) mRNA synthesis increased from the initial state at 0 h after seeding on Matrigel, reaching a steady state after 4 h. This elevated cellular t-PA mRNA level decreased markedly at 24 h. In contrast, the cellular plasminogen activator inhibitor-1 (PAI-1) mRNA level demonstrated biphasic curves during the 24 h after seeding on Matrigel: the PAI-1 mRNA level was increased eightfold initially at 4 h over that at 0 h, then declined, and again secondarily increased to greater than tenfold at 18 h. Cellular levels of both 72 kD type IV collagenase and tissue inhibitor of metalloproteinase (TIMP-2) mRNA were increased only a slightly within 2-4 h. These elevated mRNA levels were maintained for 18 h, while the TIMP-1 mRNA level increased up to 18 h, reaching around three times the level at 0 h. However, on collagen-coated dishes, cellular levels of t-PA, PAI-1, 72 kD type IV collagenase, TIMP-1, and TIMP-2 mRNA were not greatly changed during incubation for 24 h. On Matrigel, the cellular t-PA mRNA level at 18 h after seeding was greatly increased when treated with specific anti-transforming growth factor-beta (TGF-beta) antibody. In contrast, both PAI-1 and TIMP-1 mRNA levels at 18 h were reduced in the presence of anti-TGF-beta antibody. Development of the capillary network on Matrigel was inhibited in the presence of anti-t-PA antibody. Epidermal growth factor (EGF) enhanced t-PA gene expression and TGF-beta inhibited its expression in HOME cells cultured on collagen-coated dishes. On the other hand, TGF-beta enhanced cellular expression of the PAI-1 gene. The formation of a capillary network by HOME cells on Matrigel appears to be balanced by angiogenic EGF and anti-angiogenic TGF-beta through modulation of PA activity.

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Cooperative Roles of Hepatocyte Growth Factor and Plasminogen Activator in Tubular Morphogenesis by Human Microvascular Endothelial Cells

Cited by 20 publications

References 47 publications

Influence of Hepatocyte Growth Factor/Scatter Factor on the Metastatic Phenotype of B16 Melanoma Cells

Influence of Hepatocyte Growth Factor/Scatter Factor on the Metastatic Phenotype of B16 Melanoma Cells

Plasma hepatocyte growth factor is a prognostic factor in patients with acute myeloid leukemia but not in patients with myelodysplastic syndrome

Expression of tissue‐type plasminogen activator and its inhibitor couples with development of capillary network by human microvascular endothelial cells on matrigel

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