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  • 1
    ISSN: 1615-5947
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: p53 to the injured rat carotid artery. The purpose of this study was to determine if the effect of p53 gene in reducing neointimal formation would still be present up to 8 weeks after arterial injury and whether it could be enhanced by adding immunosuppression. Cytotoxic T lymphocyte–associated antigen-4 Ig (CTLA4Ig), a novel immunosuppressive agent, is a recombinant soluble protein that blocks T cell–dependent immune response. Animals were divided into eight groups (n= 6 in each). In vivo gene transfer was used in isolated segments of balloon-injured rat carotid arteries. Genetically modified adenovirus encoding for wild-type p53 protein was applied at 8 × 1010 pfu/mL. Control rats received adenovirus null at the same concentration. A daily dose of 300 μg of CTLA4Ig was given intraperitoneally, either once, twice, or three times. Expression of p53 was determined by Western blot analysis. Neointimal formation was assessed at 4 or 8 weeks by harvesting carotid arteries and determining the intima/media (I/M) ratio cross-sectional area measurements. p53 expression was confirmed by Western blot analysis. We concluded that adenovirus-mediated p53 gene transfer significantly decreases the formation of neointima up to 8 weeks following rat carotid injury. However, there is loss of effectiveness on neointimal formation inhibition as time elapses. When CTLA4Ig is added, there is significant improvement in results, with sustained neointimal formation inhibition at 8 weeks after the procedure.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Biochemistry 25 (1986), S. 2231-2237 
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-4919
    Keywords: antisense oligonucleotide ; apoptosis ; cAMP-dependent protein kinase ; cancer cells ; growth inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The enhanced expression of the RIα subunit of cyclic AMP-dependent protein kinase type 1 (PKA-I) has been correlated with cancer cell growth. We have investigated the effects of sequence-specific inhibition of RIα gene expression on the growth of MCF-7 human breast cancer cells. We report that RIα antisense treatment results in a reduction in RIα expression at both mRNA and protein levels and inhibition of cell growth. The growth inhibition was accompanied by changes in cell morphology, cleavage of poly(ADP-ribose) polymerase (PARP) and appearance of apoptotic nuclei. In addition, bcl-2 protein level was reduced and p53 expression increased in growth arrested cells. Interestingly, RIα antisense inhibited cell viability and induced apoptosis in the absence of p53, suggesting that these actions of RIα antisense are exerted independent of p53. In contrast, two- and four-base mismatched control oligonucleotides had no effect on either cell growth or morphology. These results demonstrate that the RIα antisense, which efficiently depletes the growth stimulatory molecule RIα, induces cell differentiation and apoptosis, providing a new approach to combat breast cancer cell growth.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Rat skeletal myoblasts, L6 and L8, have two major forms of phosphodiesterases, PDE II and PDE III. Only the former is activated by treatment with proteases. When the myoblasts are exposed to cAMP for 10-16 h, the activity of PDE III increases considerably. This increase is accompanied by a loss of activatability of PDE II by proteases. Leupeptin prevents the increase in the levels of PDE III suggesting that a protease in vivo may be responsible for the formation of PDE III from PDE II. Spontaneously or Rous sarcoma virus-transformed myoblasts, however, show altered regulation of the two forms of PDE. In the presence of cAMP in the medium, unlike the nontransformed cells, the levels of PDE III do not increase but the activity of PDE II rises. Simultaneously, PDE II becomes refractory to activation by proteases. The altered mode of PDE regulation in transformed cells is dominant in hybrids between normal and transformed myoblasts, which suggests that altered regulation is due to an “acquisition” of some new property by transformed cells.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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