Endothelin 1 (human, porcine)

Pluripotent stem cell-derived cardiomyocytes secrete Pro-BNP in response to small molecule-induction of cardiac hypertrophy Cardiomyocytes were treated with the vasoconstrictor, ET-1 (Endothelin-1; Catalog # 1160), or one of two L-type calcium channel inhibitors, Doxorubicin (Catalog # 2252) or Verapamil (Catalog # 0654). Levels of the cardiac hypertrophy marker, Pro-Brain Natriuretic Peptide (Pro-BNP), were detected via Luminex^® bead-based multiplex assay (Catalog # LXSAH). A substantial increase in Pro-BNP was detected in the medium of cardiomyocytes treated with ET-1, a known inducer of cardiac hypertrophy. Conversely, Doxorubicin and Verapamil decreased Pro-BNP secretion from cardiomyocytes.

Differentiated cardiomyocytes respond physiologically to Endothelin-1 induced hypertrophy Cardiomyocytes differentiated from BG01V human embryonic stem cells were treated with Endothelin-1 (ET-1; Catalog # 1160) for 28 hours to induce cardiac hypertrophy. Levels of Pro-Atrial Natriuretic peptide (Pro-ANP) secretion, which is known to be elevated during cardiac hypertrophy, were assessed using ELISA (Catalog # DANP00). As expected, detection of Pro-ANP increased proportionally with the concentration of Endothelin-1 treatment.

Endothelin Induces Expression of Atrial Natriuretic Peptide in Cardiomyocytes Derived from iPSCs JOY6 human iPSCs were differentiated into beating cardiomyocytes. After 21 days of differentiation cardiomyocytes were treated with 5 nM of Endothelin-1 (ET-1; Catalog # 1160) for 25.5 hours to induce cardiac hypertrophy. The level of secreted Pro-Atrial Natriuretic peptide (Pro-ANP), which is known to be elevated during cardiac hypertrophy, was assessed using (A) Western Blot and (B) ELISA (Human NTProANP Quantikine^® ELISA; Catalog # DANP00). As expected, detection of Pro-ANP was increased in Endothelin-1 treated cells.