Involvement of Na+/H+ exchanger in the calcium signaling in epimastigotes of Trypanosoma cruzi.

MARIANA BOLLO, SERGIO BONANSEA AND ESTELA MACHADO

FEBS LETTERS

Elseiver

Lugar: Amsterdam; Año: 2006 vol. 580 p. 2686 - 2690

0014-5793

Abstract We studied the effect of Na+ extracellular on Ca2+mobilization from intracellular store evoked by carbachol in Trypanosoma cruzi. We report that slow component of Ca2+ signaling evoked by agonist is dependent on extracellular Na+ but not on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. cruzi. We report that slow component of Ca2+ signaling evoked by agonist is dependent on extracellular Na+ but not on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. cruzi. We report that slow component of Ca2+ signaling evoked by agonist is dependent on extracellular Na+ but not on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. + extracellular on Ca2+mobilization from intracellular store evoked by carbachol in Trypanosoma cruzi. We report that slow component of Ca2+ signaling evoked by agonist is dependent on extracellular Na+ but not on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. . We report that slow component of Ca2+ signaling evoked by agonist is dependent on extracellular Na+ but not on InsP3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. P3 increase. Moreover, this Ca2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling. 2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na+/H+ exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca2+ signaling.2+ signaling. 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.