Kv1.3 is the exclusive voltage-gated K+ channel of platelets and megakaryocytes : roles in membrane potential, Ca2+ signalling and platelet count
McCloskey, Conor, Jones, Sarah, Amisten, Stefan, Snowden, Roger T., Kaczmarek, Leonard K., Erlinge, David, Goodall, Alison H., Forsythe, Ian D. and Mahaut-Smith, Martyn P.. (2010) Kv1.3 is the exclusive voltage-gated K+ channel of platelets and megakaryocytes : roles in membrane potential, Ca2+ signalling and platelet count. Journal of Physiology, Vol.588 (No.9). pp. 1399-1406. ISSN 0022-3751Full text not available from this repository.
Official URL: http://dx.doi.org/10.1113/jphysiol.2010.188136
A delayed rectifier voltage-gated K+ channel (Kv) represents the largest ionic conductance of platelets and megakaryocytes, but is undefined at the molecular level. Quantitative RT-PCR of all known Kv α and ancillary subunits showed that only Kv1.3 (KCNA3) is substantially expressed in human platelets. Furthermore, megakaryocytes from Kv1.3−/− mice or from wild-type mice exposed to the Kv1.3 blocker margatoxin completely lacked Kv currents and displayed substantially depolarised resting membrane potentials. In human platelets, margatoxin reduced the P2X1- and thromboxaneA2 receptor-evoked [Ca2+]i increases and delayed the onset of store-operated Ca2+ influx. Megakaryocyte development was normal in Kv1.3−/− mice, but the platelet count was increased, consistent with a role of Kv1.3 in apoptosis or decreased platelet activation. We conclude that Kv1.3 forms the Kv channel of the platelet and megakaryocyte, which sets the resting membrane potential, regulates agonist-evoked Ca2+ increases and influences circulating platelet numbers.
|Item Type:||Journal Article|
|Subjects:||R Medicine > R Medicine (General)|
|Divisions:||Faculty of Medicine > Warwick Medical School > Reproductive Health
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||Journal of Physiology|
|Publisher:||Wiley-Blackwell Publishing Ltd.|
|Date:||1 May 2010|
|Page Range:||pp. 1399-1406|
|Access rights to Published version:||Restricted or Subscription Access|
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