Hai-tao Zhang1, Jun Wu, Hai-feng Zhang, Qi-feng Zhu. 1. Institute of Biochemistry and Molecular Biology, Guangdong Medical College, Zhanjiang 524023, China. taohaizhang@tom.com.
Abstract
AIM: To investigate the role of intercellular potassium in tachyplesin-induced HL-60 cells apoptosis. METHODS: The concentration of intercellular potassium, cell volume and mitochondrial membrane potential were examined by flow cytometry. RESULTS: The concentration of intercellular potassium reduced in a time-dependent manner in tachyplesin-treated HL-60 cells. In addition, the loss of mitochondrial membrane potential was tightly coupled with the shrinkage of cell volume. Different caspase inhibitors protected against DNA degradation but did not prevent the loss of HL-60 cell viability induced by tachyplesin. Ba2+, which was a kind of blocker of volume-regulatory K+ channels, increased the viability of tachyplesin-treated HL-60 cells and maintained mitochondrial membrane potential and cell volume. CONCLUSION: Efflux of K+ was an important reason for apoptosis in tachyplesin-treated HL-60 cells. Efflux of K+ affected the viability of tachyplesin-treated HL-60 cells independent of the process of caspase activation.
AIM: To investigate the role of intercellular potassium in tachyplesin-induced HL-60 cells apoptosis. METHODS: The concentration of intercellular potassium, cell volume and mitochondrial membrane potential were examined by flow cytometry. RESULTS: The concentration of intercellular potassium reduced in a time-dependent manner in tachyplesin-treated HL-60 cells. In addition, the loss of mitochondrial membrane potential was tightly coupled with the shrinkage of cell volume. Different caspase inhibitors protected against DNA degradation but did not prevent the loss of HL-60 cell viability induced by tachyplesin. Ba2+, which was a kind of blocker of volume-regulatory K+ channels, increased the viability of tachyplesin-treated HL-60 cells and maintained mitochondrial membrane potential and cell volume. CONCLUSION: Efflux of K+ was an important reason for apoptosis in tachyplesin-treated HL-60 cells. Efflux of K+ affected the viability of tachyplesin-treated HL-60 cells independent of the process of caspase activation.