Genistein abolishes nucleoside uptake by cardiac fibroblasts

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dc.contributorPillai, Malini S.
dc.contributorShivakumar, K.
dc.date.accessioned2012-12-04T11:44:11Z
dc.date.available2012-12-04T11:44:11Z
dc.date.issued2009
dc.description.abstractGenistein, a soy isoflavone, is reported to exert significant beneficial action in several human disorders, which has generated immense interest in the mechanisms underlying its effects on diverse cellular processes. It has anti-proliferative action on many cell types, an effect generally attributed to tyrosine kinase inhibition. In this study, genistein was found to cause total inhibition of [(3)H]-thymidine incorporation into DNA and a modest reduction in [(3)H]-proline incorporation into protein in primary cultures of cardiac fibroblasts. The decrease in [(3)H]-thymidine incorporation was not associated with a decrease in cell proliferation but correlated exactly with low intracellular levels of [(3)H]-thymidine. Genistein dramatically reduced [(3)H]-thymidine but not [(3)H]-proline uptake by these cells in which the equilibrative nucleoside transporter may be the major route of nucleoside uptake. The effect was irreversible and was demonstrable in pulmonary fibroblasts as well. The findings suggest that nucleoside uptake mechanisms may be a novel target of genistein action in cardiac fibroblasts and point to serious limitations in using genistein to assess the role of tyrosine kinase in cell proliferation by the standard technique of [(3)H]-thymidine incorporation.
dc.identifier.citationMOLECULAR AND CELLULAR BIOCHEMISTRY. 332; 40910; 121-125en_US
dc.identifier.urihttp://dx.doi.org/10.1007/s11010-009-0181-7
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/19728041
dc.identifier.urihttps://dspace.sctimst.ac.in/handle/123456789/538
dc.publisherMOLECULAR AND CELLULAR BIOCHEMISTRY
dc.subjectCardiology
dc.titleGenistein abolishes nucleoside uptake by cardiac fibroblasts
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