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  • Endothelial cells  (1)
  • Key words Myosin heavy chain isoforms  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Induction of smooth muscle cells in the fibrous capsule of human hepatocellular carcinoma but not in the septa of hepatic cirrhosis (1999)
    Springer
    Virchows Archiv 434 (1999), S. 413-422 
    Details
    ISSN: 1432-2307
    Keywords: Key words Myosin heavy chain isoforms ; Smooth muscle actin ; Capsule ; Hepatocellular carcinoma ; Liver cirrhosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We examined the expression of smooth muscle cytoskeleton in spindle-shaped cells in the capsule of hepatocellular carcinoma (HCC) and the septa of liver cirrhosis (LC). Serial sections of livers resected from 11 patients were stained with monoclonal antibodies against vimentin, desmin, smooth muscle actin (1A4, HHF35, CGA7) and smooth muscle myosin heavy chain isoforms (SM1, SM2). Capsular spindle-shaped cells exhibited a cytoskeletal feature indicative of intermediately differentiated smooth muscle cells. Computer-assisted morphometry revealed that the proportions of 1A4-, HHF35-, CGA7- and SM1- positive areas to vimentin-positive area were 88.0±11.0%, 50.8±17.4%, 25.3±16.4% and 19.4±12.4% (n=11) in main tumours and 86.6±9.4%, 50.9±18.7%, 21.1±12.3% and 17.6±9.7% (n=12) in daughter tumours, indicating that spindle-shaped cells are heterogeneous in cytoskeletal expression. Septal spindle-shaped cells in LC lacked the cytoskeletal proteins specific to differentiated smooth muscle cells (CGA7, SM1, SM2 and desmin). Electron microscopically, capsular spindle-shaped cells contained more microfilaments and less rough endoplasmic reticulum than do septal cells. Intermediately differentiated smooth muscle cells are induced in the capsule of HCC but not in the septa of LC, suggesting a role for stromal interaction by tumour cells in the induction of smooth muscle cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050360
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Human polymorphonuclear leukocytes have dual effects on endothelin-1: The induction of endothelin-1 mRNA expression in vascular endothelial cells and modification of the endothelin-1 molecule (1993)
    Springer
    Heart and vessels 8 (1993), S. 1-6 
    Details
    ISSN: 1615-2573
    Keywords: Endothelin-1 ; Polymorphonuclear leukocytes ; Endothelial cells ; Cell-to-Cell interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of human polymorphonuclear leukocytes (PMNs) on the expression of the endothelin-1 (ET-1) gene and the production of ET-1 peptide was investigated. Human PMNs were separated from venous blood with Mono-Poly Resolving Medium and activated by incubation with formyl-methionyl-lencyl-phenylalanine (FMLP) (1 µM). Then PMN suspension was added to cultured porcine endothelial cell monolayers and coincubated for various periods. Following the coincubation, ET-1 mRNA in endothelial cells was examined by Northern blotting and immunoreactive ET-1 (irET-1) peptide levels in the conditioned media were measured by an enzyme-linked immunosorbent assay (ELISA). Similar experiments were also carried out with cell-free PMN supernatant. Untreated and activated PMNs led to a 1.4-fold and 6.3-fold increase in ET-1 mRNA levels in endothelial cells, respectively, at 6h, while irET-1 peptide levels did not significantly increase as compared with control. In contrast, when PMNs were coincubated in the presence of an Intercell chamber without direct contact to endothelial cells, PMNs did not induce ET-1 mRNA expression in endothelial cells, and significantly decreased irET-1 peptide levels in the conditioned media. Cell-free PMN supernatant did not have all these effects on ET-1. These findings suggest that direct PMN-endothelial cell contact was essential for PMN-induced expression of the ET-1 gene and that PMNs may decrease irET-1 through some modification of the ET-1 molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01744468
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    Paper (German National Licenses)
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