The nucleolus: a paradigm for cell proliferation and aging

Comai, Lucio

doi:10.1590/s0100-879x1999001200004

Cited by 24 publications

(20 citation statements)

References 45 publications

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“…This may suggest a much higher activity of the transcription/translation machinery in cryptic cells of the F344 rat colon. 34) Several other related genes were also preferentially up-regulated in the F344 strains, and taking all the results together, we consider that colon epithelial cells of F344 rats could be predisposed to a much higher level of cell proliferation than the ACI strain.…”

Section: Discussionmentioning

confidence: 71%

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

et al. 2003

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Colon cancers develop through accumulation of multiple genetic and epigenetic alterations in colon epithelial cells, and the environment of the genetically altered epithelial cells may also have a substantial impact on their further development to cancer. In the present study, groups of 6-week-old F344 and ACI male rats, the former strain being susceptible to colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and the latter being relatively resistant, were subjected to a longterm carcinogenesis experiment using our intermittent feeding protocol of PhIP in combination with a high-fat diet, which serves as a relevant risk factor that promotes the development of colon cancers. Animals were sacrificed at 60 weeks, and global gene expression analyses of normal parts of colon epithelial tissues were conducted using a high-density oligonucleotide microarray to elucidate the differential gene expression profile ( umerous studies have indicated that multiple genetic and epigenetic events are involved in the development of colon cancers. Dysregulation of the adenomatous polyposis coli (Apc), β-catenin, p53 and K-ras genes by either genetic alteration or promoter inactivation by CpG methylation plays a key role in colon carcinogenesis.

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Section: Discussionmentioning

confidence: 71%

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

et al. 2003

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“…The reduced number of AgNORs is related to the decreased nucleolar RNA transcription, ribosomal biogenesis (Likovsky´and Smetana 1981; Morimoto et al 2001) and cell proliferation activities which are known to be consistent with both aging and programmed cell death (see Kitano and Imai 1998;Comai 1999;Derenzini et al 2000;Smetana et al 2000;Campisi 2001;Smetana et al 2002). The reduced numbers and the presence of fibrillar centers corresponding to AgNORs were noted in experimentally produced apoptotic granulocytic precursors without previous terminal differentiation (Smetana et al 2004b).…”

Section: Discussionmentioning

confidence: 97%

To the intranucleolar translocation of AgNORs in leukemic early granulocytic and plasmacytic precursors

Smetana

Klamová

Pluskalová

et al. 2005

Histochem Cell Biol

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Early leukemic granulocytic and plasmacytic precursors were studied in vitro and in vivo to provide an information on the intranucleolar distribution of AgNORs (silver stained nucleolus organizer regions). In most of these cells AgNORs appeared as clusters of silver stained particles distributed in the whole nucleolar body. On the other hand, in some leukemic early granulocytic precursors, i.e., in myeloblasts and promyelocytes enlarged AgNORs were translocated in the nucleolar peripheral part. In addition, the number of translocated AgNORs at the nucleolar periphery was significantly smaller. Such translocation of a reduced number of AgNORs was easily produced by experimental aging, i.e., starving of cultured leukemic early granulocytic precursors (HL-60 and K562 cells) in vitro and seems to be reversible. Similar translocation of a reduced number of AgNORs was also produced by aging of leukemic plasmacytic precursors. Thus, the translocation of the reduced number of AgNORs to the nucleolar periphery in some blastic leukemic hematopoietic cells might be an useful marker of their aging at the single cell level. However, more studies in this direction are required in the future.

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“…Alterations in the biology of the ribosome and the nucleolus have been proposed in aging processes (27,28). Dysfunctional regulation of ribosome biogenesis would presumably have an impact on protein synthesis and thus have broad implications in cellular aging.…”

Section: Discussionmentioning

confidence: 99%

Aging results in hypermethylation of ribosomal DNA in sperm and liver of male rats

Oakes

Smiraglia

Plass

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

178

103

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There is a concern that increased paternal age may be associated with altered fertility and an increased incidence of birth defects in man. In previous studies of aged male rats, we have found abnormalities in the fertility and in the embryos sired by older males. Aging in mammals is associated with alterations in the content and patterns of DNA methylation in somatic cells; however, little is known in regard to germ cells. A systematic search for global and gene-specific alterations of DNA methylation in germ cells and liver of male rats was done. Restriction landmark genomic scanning, a method used to determine specific methylation patterns of CpG island sequences, has revealed a region of the ribosomal DNA locus that is preferentially hypermethylated with age in both spermatozoa and liver. In contrast, all single copy CpG island sequences in spermatozoa and in liver remain unaltered with age. We further demonstrate that a large proportion of rat ribosomal DNA is normally methylated and that regional and site-specific differences exist in the patterns of methylation between spermatozoa and liver. We conclude that patterns of ribosomal DNA methylation in spermatozoa are vulnerable to the same age-dependent alterations that we observe in normal aging liver. Failure to maintain normal DNA methylation patterns in male germ cells could be one of the mechanisms underlying age-related abnormalities in fertility and progeny outcome.A dvancing age in men and women has been associated with an increased incidence of parenting abnormal offspring (1). Because the father donates only chromatin to his offspring, the causal factor(s) for this effect must be of a genetic or epigenetic origin. A candidate epigenetic mechanism that may be involved in male germ cell aging is DNA methylation.The presence of 5-methylcytosine (m 5 C) in the CpG dinucleotide sequence of somatic cell DNA is commonly correlated with decreased gene expression and is also implicated in the stability of chromosomes (2). Mounting evidence links the presence of m 5 C to the recruitment of proteins to DNA that maintain stably repressed chromatin (3). In this manner, patterns of DNA methylation partition the genome into transcriptionally active and inactive regions. In mammals, the majority of cytosine bases are methylated at CpG sites. Genomic DNA is relatively CpGpoor due to an accumulation of m 5 C 3 thymine transitions. ''CpG islands'' are regions that are predominantly unmethylated and thus retain their CpG content. CpG islands are commonly found associated with genes.Age-dependent alterations of DNA methylation have been observed in mammalian somatic cells (4, 5) and occur in age-related disease (6). It is not known to what extent any of these changes may be present in germ cells. New generations of male germ cells are continually produced throughout adulthood. Age-dependent changes in DNA methylation may differ between the cells of old tissues and the cells of tissues that are renewed within an old individual. The Brown Norway (BN) rat is an inbred str...

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The nucleolus: a paradigm for cell proliferation and aging

Cited by 24 publications

References 45 publications

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

To the intranucleolar translocation of AgNORs in leukemic early granulocytic and plasmacytic precursors

Aging results in hypermethylation of ribosomal DNA in sperm and liver of male rats

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