Please use this identifier to cite or link to this item:
Title: Differential voltage-dependent K+ channel responses during proliferation and activation in macrophages
Author: Vicente García, Rubén, 1978-
Escalada, Artur
Coma, Mireia
Fuster Orellana, Gemma
Sánchez Tilló, Ester
López Iglesias, Carmen
Soler Prat, Concepció
Solsona Sancho, Carles
Celada Cotarelo, Antonio
Felipe Campo, Antonio
Keywords: Macròfags
Canals de potassi
Potassium channels
Issue Date: 21-Nov-2003
Publisher: American Society for Biochemistry and Molecular Biology
Abstract: Voltage-dependent K+ channels (VDPC) are expressed in most mammalian cells and involved in the proliferation and activation of lymphocytes. However, the role of VDPC in macrophage responses is not well established. This study was undertaken to characterize VDPC in macrophages and determine their physiological role during proliferation and activation. Macrophages proliferate until an endotoxic shock halts cell growth and they become activated. By inducing a schedule that is similar to the physiological pattern, we have identified the VDPC in non-transformed bone marrow-derived macrophages and studied their regulation. Patch clamp studies demonstrated that cells expressed outward delayed and inwardly rectifying K+ currents. Pharmacological data, mRNA, and protein analysis suggest that these currents were mainly mediated by Kv1.3 and Kir2.1 channels. Macrophage colony-stimulating factor-dependent proliferation induced both channels. Lipopolysaccharide (LPS)-induced activation differentially regulated VDPC expression. While Kv1.3 was further induced, Kir2.1 was down-regulated. TNF-alpha mimicked LPS effects, and studies with TNF-alpha receptor I/II double knockout mice demonstrated that LPS regulation mediates such expression by TNF-alpha-dependent and -independent mechanisms. This modulation was dependent on mRNA and protein synthesis. In addition, bone marrow-derived macrophages expressed Kv1.5 mRNA with no apparent regulation. VDPC activities seem to play a critical role during proliferation and activation because not only cell growth, but also inducible nitric-oxide synthase expression were inhibited by blocking their activities. Taken together, our results demonstrate that the differential regulation of VDPC is crucial in intracellular signals determining the specific macrophage response.
Note: Reproducció del document publicat a:
It is part of: Journal of Biological Chemistry, 2003, vol. 278, num. 47, p. 46307-46320
Related resource:
ISSN: 0021-9258
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
Articles publicats en revistes (Patologia i Terapèutica Experimental)
Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)
Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona))
Articles publicats en revistes (Bioquímica i Fisiologia)

Files in This Item:
File Description SizeFormat 
509471.pdf2.38 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.