2024-03-29T00:26:18Zhttps://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/445992021-06-24T07:36:44Zcom_10324_1134com_10324_931com_10324_894com_10324_32522com_10324_952com_10324_43677com_10324_954col_10324_1213col_10324_32523col_10324_43678
Characterization of ion channels involved in the proliferative response of femoral artery smooth muscle cells
Cidad Velasco, María del Pilar
Moreno Domínguez, Alejandro
Novensá, Laura
Roqué, Mercé
Barquín, Leire
Heras i Fortuny, Maria Magdalena
Pérez García, María Teresa
López López, José Ramón
Producción Científica
Objective: Vascular smooth muscle cells (VSMCs) contribute significantly to occlusive vascular diseases by virtue of their ability to switch to a noncontractile, migratory, and proliferating phenotype. Although the participation of ion channels in this phenotypic modulation (PM) has been described previously, changes in their expression are poorly defined because of their large molecular diversity. We obtained a global portrait of ion channel expression in contractile versus proliferating mouse femoral artery VSMCs, and explored the functional contribution to the PM of the most relevant changes that we observed.
Methods and Results: High-throughput real-time polymerase chain reaction of 87 ion channel genes was performed in 2 experimental paradigms: an in vivo model of endoluminal lesion and an in vitro model of cultured VSMCs obtained from explants. mRNA expression changes showed a good correlation between the 2 proliferative models, with only 2 genes, Kv1.3 and Kvβ2, increasing their expression on proliferation. The functional characterization demonstrates that Kv1.3 currents increased in proliferating VSMC and that their selective blockade inhibits migration and proliferation.
Conclusion: These findings establish the involvement of Kv1.3 channels in the PM of VSMCs, providing a new therapeutical target for the treatment of intimal hyperplasia.
2020-12-22T10:25:28Z
2020-12-22T10:25:28Z
2010
info:eu-repo/semantics/article
Arteriosclerosis, Thrombosis, and Vascular Biology, 2010, vol. 30, n. 6. p. 1203-1211
1524-4636
http://uvadoc.uva.es/handle/10324/44599
10.1161/ATVBAHA.110.205187
eng
https://www.ahajournals.org/doi/10.1161/ATVBAHA.110.205187
info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-nd/3.0/
© 2010 American Heart Association
Attribution-NonCommercial-NoDerivs 3.0 Unported
American Heart Association
SI