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Am J Physiol Cell Physiol 279: C295-C307, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 2, C295-C307, August 2000

Mechanical strain-induced Ca2+ waves are propagated via ATP release and purinergic receptor activation

H. Sauer, J. Hescheler, and M. Wartenberg

Department of Neurophysiology, University of Cologne, D-50931 Cologne, Germany

Mechanical strain applied to prostate cancer cells induced an intracellular Ca2+ (Cai2+) wave spreading with a velocity of 15 µm/s. Cai2+ waves were not dependent on extracellular Ca2+ and membrane potential because propagation was unaffected in high-K+ and Ca2+-free solution. Waves did not depend on the cytoskeleton or gap junctions because cytochalasin B and nocodazole, which disrupt microfilaments and microtubules, respectively, and 1-heptanol, which uncouples gap junctions, were without effects. Fluorescence recovery after photobleaching experiments revealed an absence of gap junctional coupling. Cai2+ waves were inhibited by the purinergic receptor antagonists basilen blue and suramin; by pretreatment with ATP, UTP, ADP, UDP, 2-methylthio-ATP, and benzoylbenzoyl-ATP; after depletion of ATP by 2-deoxyglucose; and after ATP scavenging by apyrase. Waves were abolished by the anion channel inhibitors 5-nitro-2-(3-phenylpropylamino)benzoic acid, tamoxifen, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid, niflumic acid, and gadolinium. ATP release following strain was significantly inhibited by anion channel blockers. Hence, ATP is secreted via mechanosensitive anion channels and activates purinergic receptors on the same cell or neighboring cells in an autocrine and paracrine manner, thus leading to Cai2+ wave propagation.

calcium wave; adenosine 5'-triphosphate release; purinergic receptor; anion channel


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