@article{MuenchGrivasGonzalezRajaletal.2017,
  author    = {Muench, Juliane and Grivas, Dimitrios and Gonzalez-Rajal, Alvaro and Torregrosa-Carrion, Rebeca and de la Pompa, Jos{\´e} Luis},
  title     = {Notch signalling restricts inflammation and serpine1 expression in the dynamic endocardium of the regenerating zebrafish heart},
  series = {Development : Company of Biologists},
  volume    = {144},
  journal   = {Development : Company of Biologists},
  publisher = {Company of Biologists Limited},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.143362},
  pages     = {1425 -- 1440},
  year      = {2017},
  abstract  = {The zebrafish heart regenerates after ventricular damage through a process involving inflammation, fibrotic tissue deposition/removal and myocardial regeneration. Using 3D whole-mount imaging, we reveal a highly dynamic endocardium during cardiac regeneration, including changes in cell morphology, behaviour and gene expression. These events lay the foundation for an initial expansion of the endocardium that matures to form a coherent endocardial structure within the injury site. We studied two important endocardial molecules, Serpine1 and Notch, which are implicated in different aspects of endocardial regeneration. Notch signalling regulates developmental gene expression and features of endocardial maturation. Also, Notch manipulation interferes with attenuation of the inflammatory response and cardiomyocyte proliferation and dedifferentiation. serpine1 is strongly expressed very early in the wound endocardium, with decreasing expression at later time points. serpine1 expression persists in Notch-abrogated hearts, via what appears to be a conserved mechanism. Functional inhibition studies show that Serpine1 controls endocardial maturation and proliferation and cardiomyocyte proliferation. Thus, we describe a highly dynamic endocardium in the regenerating zebrafish heart, with two key endocardial players, Serpine1 and Notch signalling, regulating crucial regenerative processes.},
  language  = {en}
}
@article{FechnerBaumannWalz2013,
  author    = {Fechner, Lennart and Baumann, Otto and Walz, Bernd},
  title     = {Activation of the cyclic AMP pathway promotes serotonin-induced Ca2+ oscillations in salivary glands of the blowfly Calliphora vicina},
  series = {Cell calcium},
  volume    = {53},
  journal   = {Cell calcium},
  number    = {2},
  publisher = {Churchill Livingstone},
  address   = {Edinburgh},
  issn      = {0143-4160},
  doi       = {10.1016/j.ceca.2012.10.004},
  pages     = {94 -- 101},
  year      = {2013},
  abstract  = {Ca2+ and cAMP signalling pathways interact in a complex manner at multiple sites. This crosstalk fine-tunes the spatiotemporal patterns of Ca2+ and cAMP signals. In salivary glands of the blowfly Calliphora vicina fluid secretion is stimulated by serotonin (5-hydroxytryptamine, 5-HT) via activation of two different 5-HT receptors coupled to the InsP(3)/Ca2+ (Cv5-HT2 alpha) or the cAMP pathway (Cv5-HT7), respectively. We have shown recently in permeabilized gland cells that cAMP sensitizes InsP(3)-induced Ca2+ release to InsP(3). Here we study the effects of the CAMP signalling pathway on 5-HT-induced oscillations in transepithelial potential (TEP) and in intracellular [Ca2+]. We show: (1) Blocking the activation of the cAMP pathway by cinanserin suppresses the generation of TEP and Ca2+ oscillations, (2) application of 8-CPT-cAMP in the presence of cinanserin restores 5-HT-induced TEP and Ca2+ oscillations, (3) 8-CPT-cAMP sensitizes the InsP(3)/Ca2+ signalling pathway to 5-HT and the Cv5-HT2 alpha, receptor agonist 5-MeOT, (4) 8-CPT-cAMP induces Ca2+ oscillations in cells loaded with subthreshold concentrations of InsP(3), (5) inhibition of protein kinase A by H-89 abolishes 5-HT-induced TEP and Ca2+ spiking and mimics the effect of cinanserin. These results suggest that activation of the cyclic AMP pathway promotes the generation of 5-HT-induced Ca2+ oscillations in blowfly salivary glands.},
  language  = {en}
}