Manipulating intracellular Ca2+ signals to stimulate therapeutic angiogenesis in cardiovascular disorders.

Manipulating intracellular Ca2+ signals to stimulate therapeutic angiogenesis in cardiovascular disorders. Curr Pharm Biotechnol. 2018 Aug 08;: Authors: Moccia F, Berra-Romani R, Rosti V Abstract Endothelial progenitor cells (EPCs) are mobilized in peripheral blood to rescue blood perfusion in ischemic tissues. Several approaches were, therefore, designed to inject autologous EPCs and induce therapeutic angiogenesis in patients affected by cardiovascular disorders. Endothelial colony forming cells (ECFCs) represent the only truly endothelial precursor and are regarded as the most suitable substrate for cell based therapy of ischemic diseases. Intracellular Ca2+ signalling drives ECFC proliferation, migration, homing and neovessel formation. Vascular endothelial growth factor (VEGF) triggers repetitive oscillations in intracellular Ca2+ concentration ([Ca2+]i) in peripheral blood- and umbilical cord blood-derived ECFCs by initiating a dynamic interplay between inositol-1,4,5-trisphosphate (InsP3)-dependent Ca2+ release and store-operated Ca2+ entry (SOCE). SOCE, in turn, is mediated by Stim1, Orai1 and Transient Receptor Potential (TRP) Canonical 1 (TRPC1). Intriguingly, intracellular Ca2+ oscillations are triggered by TRPC3 in umbilical cord blood-derived ECFCs, which display higher proliferative potential. Additionally, stromal cell-derived factor-1a (SDF-1a) triggers a biphasic increase in [Ca2+]i in ECFCs which is mediated by InsP...
Source: Current Pharmaceutical Biotechnology - Category: Biotechnology Authors: Tags: Curr Pharm Biotechnol Source Type: research