Effects of Colchicine on Apoptotic Cell Death of Cardiomyocytes

Objectives: We wished to examine the effects of colchicine, currently on clinical trials for acute myocardial infarction (AMI), on the viability of cardiac cells using a cell line model AMI.

Methods: Murine cardiomyocyte cell line, HL-1 and rat cardiomyoblast cell line, H9C2, were incubated with TNFα or with sera derived from rats that underwent AMI or sham-operation followed by addition of colchicine. In another experiment, HL-1/H9C2 cells were exposed to anoxia with or without subsequent addition of colchicine. Cellular morphology and viability were assessed by light microscopy, flow cytometry and Western analyses for apoptotic markers.

Results: Cellular viability was similar with both sera; however, exposing both cell lines to anoxia reduced their viability. Adding colchicine to anoxic H9C2, but not to anoxic HL-1, further increased their mortality, at least in part via enhanced apoptosis. Under any condition, colchicine induced detachment of H9C2 cells from their culture plates. This phenomenon did not apply to HL-1 cells.

Conclusions: Colchicine enhanced mortality of cardiomyoblasts under in vitro conditions mimicking AMI and reduced their adherence capability. HL-1 was not affected by colchicine; nevertheless, no salvage effect was observed. We thus conclude that colchicine may not inhibit myocardial apoptosis following AMI.