Institute of Physiology Neuropathophysiology

Münster, Germany

Institute of Physiology Neuropathophysiology

Münster, Germany

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Bobak N.,University of Munster | Bobak N.,Institute of Physiology Neuropathophysiology | Bittner S.,University of Munster | Bittner S.,Institute of Physiology Neuropathophysiology | And 20 more authors.
Biochimica et Biophysica Acta - Biomembranes | Year: 2011

A variety of ion channels are supposed to orchestrate the homoeostatic volume regulation in T lymphocytes. However, the relative contribution of different potassium channels to the osmotic volume regulation and in particular to the regulatory volume decrease (RVD) in T cells is far from clear. This study explores a putative role of the newly identified K2P channels (TASK1, TASK2, TASK3 and TRESK) along with the voltage-gated potassium channel KV1.3 and the calcium-activated potassium channel KCa3.1 in the RVD of murine T lymphocytes, using genetic and pharmacological approaches. K2P channel knockouts exerted profound effects on the osmotic properties of murine T lymphocytes, as revealed by reduced water and RVD-related solute permeabilities. Moreover, both genetic and pharmacological data proved a key role of KV1.3 and TASK2 channels in the RVD of murine T cells exposed to hypotonic saline. Our experiments demonstrate a leading role of potassium channels in the osmoregulation of T lymphocytes under different conditions. In summary, the present study sheds new light on the complex and partially redundant network of potassium channels involved in the basic physiological process of the cellular volume homeostasis and extends the repertoire of potassium channels by the family of K2P channels. © 2011 Elsevier B.V.

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