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  • Hepatocytes Dietary restriction Cell proliferation Apoptosis Bromodeoxyuridine incorporation Proliferating cell nuclear antigen Terminal dUTP nick end labeling (TUNEL) TGFα TGFβ1 p53 Fas TNF receptor Rat (Fischer 344)  (1)
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    ISSN: 1432-0878
    Keywords: Hepatocytes Dietary restriction Cell proliferation Apoptosis Bromodeoxyuridine incorporation Proliferating cell nuclear antigen Terminal dUTP nick end labeling (TUNEL) TGFα TGFβ1 p53 Fas TNF receptor Rat (Fischer 344)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Dietary restriction (DR) retards physical growth, resulting in small body size, reduced liver weight and reduced number of hepatocytes in rats. We examined the effects of DR on proliferation and apoptosis of hepatocytes during development and explained these changes subcellularly using immunohistochemistry for bromodeoxyuridine (BrdU) incorporation, proliferating cell nuclear antigen (PCNA) and p53, terminal dUTP nick end labeling (TUNEL) and quantitative reverse transcription-polymerase chain reaction (RT-PCR) for TGFα, TGFβ1, p53, Fas and TNF receptor (TNFr). Tissue samples included the livers of 3-month-old male Fischer 344 rats fed ad libitum (AL) or on 70% DR. DR significantly reduced the proportions of BrdU-positive and PCNA-strongly-positive hepatocytes compared with AL rats but not the proportions of PCNA-positive hepatocytes and TUNEL-positive hepatocytes. On the other hand, DR enhanced the expression of p53 and Fas mRNAs but failed to influence the expression of TGFα, TGFβ1 and TNFr mRNAs. Moreover, DR significantly increased the proportion of p53-positive hepatocytes. Our findings suggest that DR suppresses the proliferation of hepatocytes, resulting in a reduced number of hepatocytes during development. This process may be mediated by overexpression of p53 suppressor gene. While DR accelerates the expression of Fas antigen, this result does not influence the rate of apoptosis of hepatocytes under physiological conditions.
    Type of Medium: Electronic Resource
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