Ca2+-Activated K Channel of the BK-Type in the Inner Mitochondrial Membrane of a Human Glioma Cell Line

Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes

“…Activation of plasma membrane Kv1.3 is intimately involved in T cell proliferation and maturation (7), but studies employing actinomycin D to induce cell death also suggest the importance of Kv1.3 in apoptosis (8). We have recently reported that, like other channels expressed in multiple subcellular locations (9)(10)(11)(12), the potassium channel Kv1.3 is present in a functionally active form not only in the plasma membrane, but also in the IMM of lymphocytes (13). The present study demonstrates that IMM Kv1.3 interacts with Bax in a toxin-like mode to trigger cell death.…”

Role of epoxyeicosatrienoic acids in protecting the myocardium following ischemia/reperfusion injury

“…CYP epoxygenase derived EETs are known activators of BK Ca channels in vascular smooth muscle [20,67], whereas, CYP ω-hydroxylases derived HETEs are known inhibitors in vascular smooth muscle [38,68,69]. Recent evidence suggests that newly identified K Ca channels in cardiac mitochondria (mito K Ca ) [53,70] are important mediators of cardioprotection. It is proposed that these mitochondrial K + channels work in concert with mito K ATP and other mitochondrial proteins in response to ischemia [49].…”

“…Activation of K + channels by kinases, such as PKC or PKA, and other unknown signals is predicted to increase mitochondrial K + uptake and in turn reduce Ca 2+ overload in cardiomyocytes. The cardioprotective mechanisms associated with opening of these channels include a mild uncoupling, depolarization of the intramitochondrial membrane, transient swelling of the intramitochondrial space, enhanced respiration via the electron transport chain and altered production of reactive oxygen species [49,53,59,60,64,70].…”

Mitochondrial calcium handling during ischemia-induced cell death in neurons

“…Whether mitochondrial ATPsensitive potassium channels are present in brain and play a role during cerebral ischemia is disputed [108e110], but electrophoretic potassium flux in brain mitochondria is well established [111] and a voltage-gated potassium channel (Kv1.3) has been electrophysiologically characterized in gerbil hippocampal mitochondria [112]. More relevant, two Ca 2þ -activated potassium channels (K Ca 1.1 and K Ca 3.1) have been detected in inner mitochondrial membrane and characterized by mitochondrial patch-clamp [113,114]. The large conductance Ca 2þ -activated potassium channels (BK Ca or K Ca 1.1) is present in mitochondria from glioma cells [113] and from rat brain [115], and has been proposed to contribute to the cardioprotective effect of potassium influx into mitochondria [116] accumulation and PTP opening is well established, and despite the fact that MPT invariably leads to neuronal cell death, these relationships do not necessarily imply that matrix Ca 2þ accumulation is directly responsible for the injuries related to cerebral ischemia.…”

“…More relevant, two Ca 2þ -activated potassium channels (K Ca 1.1 and K Ca 3.1) have been detected in inner mitochondrial membrane and characterized by mitochondrial patch-clamp [113,114]. The large conductance Ca 2þ -activated potassium channels (BK Ca or K Ca 1.1) is present in mitochondria from glioma cells [113] and from rat brain [115], and has been proposed to contribute to the cardioprotective effect of potassium influx into mitochondria [116] accumulation and PTP opening is well established, and despite the fact that MPT invariably leads to neuronal cell death, these relationships do not necessarily imply that matrix Ca 2þ accumulation is directly responsible for the injuries related to cerebral ischemia. The group of Lemasters, for example, has proposed that mitochondrial Ca 2þ overload is a consequence, rather than a cause, of the bioenergetic failure that follows MPT onset.…”