RT info:eu-repo/semantics/article
T1 Contribution of Kv channels to phenotypic remodeling of human uterine artery smooth muscle cells
A1 Miguel Velado, Eduardo
A1 Moreno Domínguez, Alejandro
A1 Colinas, Olaia
A1 Cidad Velasco, María del Pilar
A1 Heras i Fortuny, Maria Magdalena
A1 Pérez García, María Teresa
A1 López López, José Ramón
K1 Potassium channels
K1 Canales de potasio
K1 Vascular smooth muscle
K1 Músculo liso vascular
K1 Cell proliferation
K1 Proliferación celular
AB Vascular smooth muscle cells (VSMCs) perform diverse functions that can be classified into contractile and synthetic (or proliferating). All of these functions can be fulfilled by the same cell because of its capacity of phenotypic modulation in response to environmental changes. The resting membrane potential is a key determinant for both contractile and proliferating functions. Here, we have explored the expression of voltage-dependent K+ (Kv) channels in contractile (freshly dissociated) and proliferating (cultured) VSMCs obtained from human uterine arteries to establish their contribution to the functional properties of the cells and their possible participation in the phenotypic switch. We have studied the expression pattern (both at the mRNA and at the protein level) of Kvα subunits in both preparations as well as their functional contribution to the K+ currents of VSMCs. Our results indicate that phenotypic remodeling associates with a change in the expression and distribution of Kv channels. Whereas Kv currents in contractile VSMCs are mainly performed by Kv1 channels, Kv3.4 is the principal contributor to K+ currents in cultured VSMCs. Furthermore, selective blockade of Kv3.4 channels resulted in a reduced proliferation rate, suggesting a link between Kv channels expression and phenotypic remodeling.
PB American Heart Association
SN 1524-4571
YR 2005
FD 2005
LK http://uvadoc.uva.es/handle/10324/44600
UL http://uvadoc.uva.es/handle/10324/44600
LA eng
NO Circulation Research, 2005, vol. 97, n. 12. p. 1280-1287
NO Producción Científica
DS UVaDOC
RD 23-abr-2024