A study of the extracellular matrix protein as the migration pathway of neural crest cells in the gut: Analysis in human embryos with special reference to the pathogenesis of Hirschsprung's disease

Fujimoto, Toshio; Hata, Junichi; Yokoyama, Sho; Mitomi, Toshio

doi:10.1016/s0022-3468(89)80504-4

Cited by 64 publications

(21 citation statements)

References 9 publications

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“…14 and 25). HA is a linear anionic polymer comprised of a single repeating disaccharide motif critical for regulating cell division, cell motility, and cellular transformation during development (51)(52)(53)(54)(55)(56)(57)(58). HA polymers and HA oligosaccharides have been implicated in distinct aspects of these processes.…”

Section: Discussionmentioning

confidence: 99%

Inducible Hyaluronan Production Reveals Differential Effects on Prostate Tumor Cell Growth and Tumor Angiogenesis

Bharadwaj

Rector

Simpson

2007

Journal of Biological Chemistry

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Prostate cancer progression can be predicted in human tumor biopsies by abundant hyaluronan (HA) and its processing enzyme, the hyaluronidase HYAL1. Accumulation of HA is dictated by the balance between expression levels of HA synthases, the enzymes that produce HA polymers, and hyaluronidases, which process polymers to oligosaccharides. Aggressive prostate tumor cells express 20-fold higher levels of the hyaluronan synthase HAS3, but the mechanistic relevance of this correlation has not been determined. We stably overexpressed HAS3 in prostate tumor cells. Adhesion to extracellular matrix and cellular growth kinetics in vitro were significantly reduced. Slow growth in culture was restored either by exogenous addition of hyaluronidase or by stable HYAL1 coexpression. Coexpression did not improve comparably slow growth in mice, however, suggesting that excess hyaluronan production by HAS3 may alter the balance required for induced tumor growth. To address this, we used a tetracycline-inducible HAS3 expression system in which hyaluronan production could be experimentally controlled. Adjusting temporal parameters of hyaluronan production directly affected growth rate of the cells. Relief from growth suppression in vitro but not in vivo by enzymatic removal of HA effectively uncoupled the respective roles of hyaluronan in growth and angiogenesis, suggesting that growth mediation is less critical to establishment of the tumor than early vascular development. Collectively results also imply that HA processing by elevated HYAL1 expression in invasive prostate cancer is a requirement for progression.Despite improved detection and diagnosis of prostate cancer, this disease remains the second leading cause of malignant mortality in United States males (1, 2). Metastasis may occur with no prior indication of an invasive tumor (3), so prostate cancer progression is difficult to predict. Changes in levels of extracellular matrix molecules such as hyaluronan (HA), 2 a high molecular weight polysaccharide, and its processing enzyme, the hyaluronidase HYAL1, within the prostate extracellular matrix have been correlated to invasive prostate cancer progression (4 -11). The molecular mechanisms underlying this correlation could provide important insights for therapeutic development or improved diagnosis of prostate cancer.HA production is a tightly regulated process that impacts cellular transformation and motility during development (12)(13)(14). Dynamic HA turnover within tissues controls many acute processes such as wound healing or immune function. HA accumulation is the outcome of a balance between the activity of HA synthases (HAS), enzymes that synthesize the linear polymers (15), and hyaluronidases, which process the polymers to biologically potent oligosaccharides (16). Excess quantities of large HA polymers have been reported to suppress cellular growth (17, 18) and angiogenesis (19,20), whereas processed oligosaccharides dramatically stimulate angiogenesis (21-23), and fully degraded oligosaccharides induce apoptosis (1...

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Section: Discussionmentioning

confidence: 99%

Inducible Hyaluronan Production Reveals Differential Effects on Prostate Tumor Cell Growth and Tumor Angiogenesis

Bharadwaj

Rector

Simpson

2007

Journal of Biological Chemistry

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“…HA is required for normal ductal branching in the developing prostate gland (46), underscoring its vital role in cell migration (47). In some cell types, this requirement entails assembly of an HA pericellular matrix for proliferation and migration (33,48).…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan Synthase Elevation in Metastatic Prostate Carcinoma Cells Correlates with Hyaluronan Surface Retention, a Prerequisite for Rapid Adhesion to Bone Marrow Endothelial Cells

Simpson¹,

Reiland²,

Burger³

et al. 2001

Journal of Biological Chemistry

100

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Bone marrow is the primary site of metastasis in patients with advanced stage prostate cancer. Prostate carcinoma cells metastasizing to bone must initially adhere to endothelial cells in the bone marrow sinusoids. In this report, we have modeled that interaction in vitro using two bone marrow endothelial cell (BMEC) lines and four prostate adenocarcinoma cell lines to investigate the adhesion mechanism. Highly metastatic PC3 and PC3M-LN4 cells were found to adhere rapidly and specifically (70 -90%) to BMEC-1 and trHBMEC bone marrow endothelial cells, but not to human umbilical vein endothelial cells (15-25%). Specific adhesion to BMEC-1 and trHBMEC was dependent upon the presence of a hyaluronan (HA) pericellular matrix assembled on the prostate carcinoma cells. DU145 and LNCaP cells were only weakly adherent and retained no cell surface HA. Maximal BMEC adhesion and HA encapsulation were associated with high levels of HA synthesis by the prostate carcinoma cells. Up-regulation of HA synthase isoforms Has2 and Has3 relative to levels expressed by normal prostate corresponded to elevated HA synthesis and avid BMEC adhesion. These results support a model in which tumor cells with up-regulated HA synthase expression assemble a cell surface hyaluronan matrix that promotes adhesion to bone marrow endothelial cells. This interaction could contribute to preferential bone metastasis by prostate carcinoma cells.

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“…For example, soluble factors that have been shown to regulate different aspects of ENCC biology in vitro are present locally along the rostrocaudal axis of the embryonic gut (Chalazonitis et al, 2004;Leibl et al, 1999;Woodward et al, 2000;Barlow et al, 2003;Natarajan et al, 2002;Anderson et al, 2007). In addition, several extracellular matrix (ECM) components are present in the gut wall during or after the gut colonisation by ENCCs, although variations in their expression patterns along the rostrocaudal axis of the gut have not been extensively analysed (Fujimoto et al, 1989;Newgreen and Hartley, 1995;Lefèbvre et al, 1999;Scherberich et al, 2004;Simon-Assmann et al, 1995;Bolcato-Bellemin et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

β1 integrins are required for the invasion of the caecum and proximal hindgut by enteric neural crest cells

et al. 2009

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Integrins are the major adhesive receptors for extracellular matrix and have various roles in development. To determine their role in cell migration, the gene encoding the β1 integrin subunit (Itgb1) was conditionally deleted in mouse neural crest cells just after their emigration from the neural tube. We previously identified a major defect in gut colonisation by conditional Itgb1-null enteric neural crest cells (ENCCs) resulting from their impaired migratory abilities and enhanced aggregation properties. Here, we show that the migration defect occurs primarily during the invasion of the caecum, when Itgb1-null ENCCs stop their normal progression before invading the caecum and proximal hindgut by becoming abnormally aggregated. We found that the caecum and proximal hindgut express high levels of fibronectin and tenascin-C, two well-known ligands of integrins. In vitro, tenascin-C and fibronectin have opposite effects on ENCCs, with tenascin-C decreasing migration and adhesion and fibronectin strongly promoting them. Itgb1-null ENCCs exhibited an enhanced response to the inhibitory effect of tenascin-C, whereas they were insensitive to the stimulatory effect of fibronectin. These findings suggest that β1 integrins are required to overcome the tenascin-C-mediated inhibition of migration within the caecum and proximal hindgut and to enhance fibronectin-dependent migration in these regions.

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A study of the extracellular matrix protein as the migration pathway of neural crest cells in the gut: Analysis in human embryos with special reference to the pathogenesis of Hirschsprung's disease

Cited by 64 publications

References 9 publications

Inducible Hyaluronan Production Reveals Differential Effects on Prostate Tumor Cell Growth and Tumor Angiogenesis

Inducible Hyaluronan Production Reveals Differential Effects on Prostate Tumor Cell Growth and Tumor Angiogenesis

Hyaluronan Synthase Elevation in Metastatic Prostate Carcinoma Cells Correlates with Hyaluronan Surface Retention, a Prerequisite for Rapid Adhesion to Bone Marrow Endothelial Cells

β1 integrins are required for the invasion of the caecum and proximal hindgut by enteric neural crest cells

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