Isolated cardiomyocytes were perfused with 10-8 M isoproterenol (Sigma-Aldrich, Madrid, Spain) for 1–5 min and intracellular Ca2+ dynamics were recorded. In some experiments, cells were pretreated with the selective NOD1 agonist C12-iE-DAP (iE-DAP, InvivoGen, San Diego, CA, United States), which has significant cell membrane permeability and high potency (Fernández-Velasco et al., 2012 (link); Delgado et al., 2015 (link); Val-Blasco et al., 2017a (link)), or iE-Lys (Invivogen), an inactive analog of NOD1. Nodinitib-1 (Cayman) was used as a selective NOD1 inhibitor and mice were injected IP with 5 μmol/L Nodinitib-1 or vehicle (<0.01% DMSO) three times weekly for 6 weeks.
Val-Blasco A., Navarro-García J.A., Tamayo M., Piedras M.J., Prieto P., Delgado C., Ruiz-Hurtado G., Rozas-Romero L., Gil-Fernández M., Zaragoza C., Boscá L, & Fernández-Velasco M. (2018). Deficiency of NOD1 Improves the β-Adrenergic Modulation of Ca2+ Handling in a Mouse Model of Heart Failure. Frontiers in Physiology, 9, 702.
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