Key result
Transient focal cerebral ischemia increases Kv2.1 expression ~50% early after reperfusion.
Effect estimate: 1.53-fold increase in mRNA; 1.49-fold increase in protein
p-value: p=<0.01
Kv2.1 potassium channel expression transiently increases during the early period of focal cerebral ischemia in mice, suggesting a role in neuronal potassium homeostasis.
Objective: Potassium channels play an essential role in neuronal potassium homeostasis. Kv2.1 is widely expressed in the mammalian brain and it undergoes dramatic functional modulation during brain ischemia. This study characterized the serial changes in brain Kv2.1 expression after transient focal cerebral ischemia in mice.Methods: C57BL/6 mice (n=45) were subjected to 60 min of middle cerebral artery occlusion followed by 1, 1.5, 2, and 3 h reperfusion. Hypoxic area was determined by hypoxyprobe-1 and Kv2.1 expression was measured by real-time PCR, immunofluorescence imaging, and western blotting.Results: Kv2.1 mRNA increased 1 h after cerebral ischemia-reperfusion injury, and then decreased. In western blotting, expression of Kv2.1 protein decreased at 1 h and decreased Kv2.1 protein level turned to peak level of Kv2.1 expression at 1.5 h. In immunohistochemistry revealed a gradual increase in Kv2.1 at 1.5 h after reperfusion. Conclusions: Kv2.1 expression transiently increased after cerebral ischemia. Our results suggest Kv2.1 may play an important role in potassium transport during the early period of focal cerebral ischemia.
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Mitsuhashi et al. (2014) studied Focal cerebral ischemia (n=45). Transient focal cerebral ischemia (MCAO) vs. Sham operation was evaluated on Kv2.1 mRNA and protein expression in the ischemic cerebral cortex (1.53-fold increase in mRNA; 1.49-fold increase in protein, p=<0.01). Transient focal cerebral ischemia significantly increased Kv2.1 mRNA expression by 1.53-fold at 1 hour and Kv2.1 protein expression by 1.49-fold at 1.5 hours after reperfusion.
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