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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.
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Verapamil affects cardiomyocyte contraction rates.
The effect of small molecules on cardiomyocyte contraction rate was assessed by monitoring intracellular calcium fluctuations, where an increase in calcium coincides with cardiomyocyte contraction. Cardiomyocytes were loaded with the fluorescent calcium indicator, Fluo-4, prior to small molecule treatment. Individual wells were first monitored for baseline rates of calcium fluctuation represented as beats per minute (bpm). Verapamil (10uM or 30uM, Catalog # 0654), an L-type calcium channel blocker, decreased the rate of calcium fluctuations in cardiomyocytes in a dose-dependent manner.
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