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This Article Full Text Full Text (PDF) All Versions of this Article: 576/1/179    most recent jphysiol.2006.111278v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Podgorska, M. Articles by Pawelczyk, T. Search for Related Content PubMed PubMed Citation Articles by Podgorska, M. Articles by Pawelczyk, T. Related Collections Cardiovascular

Departments of
¹ Molecular Medicine
² Laboratory Medicine, Medical University of Gdansk, 80-211 Gdansk, Poland

Adenosine produced by cardiac cells is known to attenuate the proliferation of cardiac fibroblasts (CFs), inhibit collagen synthesis, and protect the myocardium against ischaemic and reperfusion injury. Diabetic patients' hearts exhibit ventricular hypertrophy and demonstrate reduced tolerance to hypoxia or ischaemia. In this study, we characterize the effects of glucose and insulin on processes that determine the release of adenosine from CFs. We showed that during ATP depletion, rat CFs cultured in the absence of insulin release significantly less adenosine compared to cells grown in the presence of insulin. Moreover, under both conditions the quantity of released adenosine depends on glucose concentration. We demonstrate that this is due to altered expression of nucleoside transporters. High glucose (25 mM) induced 85% decrease in nucleoside transporter ENT1 mRNA levels. Decrease of the insulin level below 10^–11 M resulted in over 3-fold increase in the nucleoside transporter CNT2 mRNA content. Measurements of adenosine transport in CFs cultured in the presence of 5 mM glucose and 10 nM insulin showed that the bidirectional equilibrative adenosine transport accounted for 70% of the overall adenosine uptake. However, cells grown in the presence of high glucose (25 mM) demonstrated 65% decrease of the bidirectional equilibrative adenosine transport. Experiments on CFs cultured in the absence of insulin showed that the unidirectional Na⁺-dependent adenosine uptake rose in these cells more than 4-fold. These results indicate that the development of diabetes may result in an increased uptake of interstitial adenosine by CFs, and reduction of the ability of these cells to release adenosine during ATP deprivation.

(Received 10 April 2006; accepted after revision 19 July 2006; first published online 27 July 2006)
Corresponding author T. Pawelczyk: Department of Molecular Medicine, Medical University of Gdansk, ul. Debinki 7, paw. 29, 80-211 Gdansk, Poland. Email: tkpaw{at}amg.gda.pl

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