title: The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver.
abstract: Neutrophils are phagocytic cells that play a critical role in innate immunity by destroying bacterial pathogens. Channels belonging to the inward rectifier potassium channel subfamily 2 (Kir2 channels) have been described in other phagocytes (monocytes/macrophages and eosinophils) and in hematopoietic precursors of phagocytes. Their physiological function in these cells remains unclear, but some evidence suggests a role in growth factor-dependent proliferation and development. Expression of functional Kir2 channels has not been definitively demonstrated in mammalian neutrophils. Here, we show by RT-PCR that neutrophils from mouse bone marrow and liver express mRNA for the Kir2 subunit Kir2.1 but not for other subunits (Kir2.2, Kir2.3, and Kir2.4). In electrophysiological experiments, resting (unstimulated) neutrophils from mouse bone marrow and liver exhibit a constitutively active, external K(+)-dependent, strong inwardly rectifying current that constitutes the dominant current. The reversal potential is dependent on the external K(+) concentration in a Nernstian fashion, as expected for a K(+)-selective current. The current is not altered by changes in external or internal pH, and it is blocked by Ba(2+), Cs(+), and the Kir2-selective inhibitor ML133. The single-channel conductance is in agreement with previously reported values for Kir2.1 channels. These properties are characteristic of homomeric Kir2.1 channels. Current density in short-term cultures of bone marrow neutrophils is decreased in the absence of growth factors that are important for neutrophil proliferation [granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF)]. These results demonstrate that mouse neutrophils express functional Kir2.1 channels and suggest that these channels may be important for neutrophil function, possibly in a growth factor-dependent manner.
authors.affiliation: Department of Pathology and Laboratory Medicine, Massachusetts General Hospital, Boston, Massachusetts; and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts rmasia@mgh.harvard.edu.
authors.forename: Ricard
authors.initials: R
authors.lastname: Masia
authors.affiliation: Department of Pathology and Laboratory Medicine, Massachusetts General Hospital, Boston, Massachusetts; and.
authors.forename: Daniela S
authors.initials: DS
authors.lastname: Krause
authors.affiliation: Department of Neurobiology, Harvard Medical School, Boston, Massachusetts.
authors.forename: Gary
authors.initials: G
authors.lastname: Yellen
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000378:metabolism*; D002478:Cells, Cultured; D005260:Female; D005786:Gene Expression Regulation; D008099:Liver / Q000166:cytology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000096:biosynthesis*
chemical_list: C489461:Kir2.1 channel; D024661:Potassium Channels, Inwardly Rectifying
keywords: Kir2 channels; granulocyte colony-stimulating factor; inward rectifier potassium channel; neutrophil