The impaired transcription factor AP-1 DNA binding activity in lymphocytes derived from subjects with some symptoms of premature ageing

• Autorzy: Sikora E. , Radziszewska E. , Kmiec T. , Maslinska D.
• Języki publikacji: EN

Abstrakty

The study of human disorders known as premature aging syndromes may provide insight into the mechanisms of cellular senescence. The main feature of cellular senescence in vitro is cessation of cell proliferation. Down syndrome (DS) and neuronal ceroid-lypofuscinosis (NCL) are clinically characterized by the premature onset of numerous features normally associated with human aging. Phytohemagglu- tinin stimulated lymphocytes derived from DS subjects showed a statistically significant diminished proliferation capacity in comparison with lymphocytes derived from NCL and healthy individuals. We demonstrated, by applying the electrophoretic mobility shift assay, slightly impaired AP-1 DNA binding activity in NCL lymphocytes and strong in DS ones. Our results showed that the same molecular mechanisms of proliferation cessation could exist in fibroblasts characterized by replicative senescence and in lymphocytes derived from individuals with premature aging syndromes (Down).

Słowa kluczowe

EN

transcription factor; lymphocyte; premature aging; DNA binding; aging

• Wydawca: -
• Czasopismo: Acta Biochimica Polonica
• Rocznik: 1993
• Tom: 40
• Numer: 2
• Opis fizyczny: p.269-272,fig.

Twórcy

autor

Sikora E.

• Nencki Institute of Experimental Biology, Pasteura 3, 02-093 Warsaw, Poland

autor

Radziszewska E.

autor

Kmiec T.

autor

Maslinska D.

Bibliografia

• 1. Goldstein, S. (1990) Replicative senescence: the human fibroblast comes of age. Science 249,1129 -1133.
• 2. Rittling, S.R., Brooks, K.M., Cristofalo, V.J. & Baserga, R. (1986) Expression of cell cycle-de- pendent genes in young and senescent WI-38 fibroblasts. Proc. Natl. Acad. Sci. U.S.A. 83,3316 -3320.
• 3. Seshadri, T. & Campisi, J. (1990) Repression of c-fos transcription and an altered genetic program in senescent human fibroblasts. Science 247,205 - 208.
• 4. Angel, P. & Karin, M. (1991) The role of Jun, Fos and AP-1 complex in cell-proliferation and transformation. Biochitn. Biophys. Acta 1072,129 -157.
• 5. Riabowol, K., Schiff, J. & Gilman, M.Z. (1992) Transcription factor AP-1 activity is required for initiation of DNA synthesis and is lost during cellular aging. Proc. Natl. Acad. Sci. U.S.A. 89,157 -161.
• 6. Sikora, E., Kamińska, B., Radziszewska, E. & Kaczmarek, L. (1992) Loss of transcription factor AP-1 DNA binding activity during lymphocyte aging in vivo. FEBS Lett. 312,179 - 182.
• 7. Miller, R. (1991) Aging and immune function. Int. Rev. Cytol. 124,187 - 211.
• 8. Cossarizza, A., Monti, D., Montagniani, G., Ortolani, C., Masi, M., Zannotti, M. & Franceschi, C. (1990) Precocious aging of the immune system in Down Syndrome. Am. J. Med. Genet. Suppl. 7,213 - 218.
• 9. Zeman, W.( 1971) The neuronal ceroid-lipofu­scinoses Batten-Vogt syndrome; a model for human aging? Adv. Gerontol. Res. 3,147 -170.
• 10. Santavuori, P. (1988) Neuronal ceroid-lipofu­scinoses in childhood. Brain Develop. 10,80 - 83.
• 11. Schreiber, E., Matthis, P., Muller, M.M. & Schaffner, W. (1989) Rapid detection of octamer binding proteins with 'mini-extracts' prepared from a small number of cells. Nucleic Acids Res. 17,15.
• 12. Bradford, M.M. (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem. 72,248 - 254.