dc.creator | González Montelongo, M. Carmen | es |
dc.creator | Porras González, Cristina | es |
dc.creator | González Montelongo, Rafaela | es |
dc.creator | Revilla González, Gonzalo | es |
dc.creator | Pastor, María Dolores | es |
dc.creator | Castellano Orozco, Antonio Gonzalo | es |
dc.creator | Ureña López, Juan | es |
dc.date.accessioned | 2021-04-22T08:13:48Z | |
dc.date.available | 2021-04-22T08:13:48Z | |
dc.date.issued | 2019-02-18 | |
dc.identifier.citation | González Montelongo, M.C., Porras González, C., González Montelongo, R., Revilla González, G., Pastor, M.D., Castellano, A. y Ureña, J. (2019). PKCα-Mediated Downregulation of RhoA Activity in Depolarized Vascular Smooth Muscle: Synergistic Vasorelaxant Effect of PKCα and ROCK Inhibition. Cellular Physiology And Biochemistry, 52 (1), 76-93. | |
dc.identifier.issn | 1015-8987 | es |
dc.identifier.uri | https://hdl.handle.net/11441/107535 | |
dc.description.abstract | Background/Aims: Protein kinase C (PKC)- and RhoA/Rho-associated kinase (ROCK)
play important roles in arterial sustained contraction. Although depolarization-elicited
RhoA/ROCK activation is accepted, the role of PKC in depolarized vascular smooth muscle
cells (VSMCs) is a subject of controversy. Our aim was to study the role of PKC in arterial
contraction and its interaction with RhoA/ROCK. Methods: Mass spectrometry was used to
identify the PKC isoenzymes. PKCα levels and RhoA activity were analyzed by western blot
and G-LISA, respectively, and isometric force was measured in arterial rings. Results: In
depolarized VSMCs RhoA and PKCα were translocated to the plasma membrane, where they
colocalize and coimmunoprecipitate. Interestingly, depolarization-induced RhoA activation
was downregulated by PKCα, effect reverted by PKCα inhibition. Phorbol 12,13-dibutyrate
(PDBu) induced the translocation of PKCα to the plasma membrane, increased the level of
RhoA in the cytosol and reduced RhoA/ROCK activity. These effects were reverted when PKC
was inhibited. Pharmacological or siRNA inhibition of PKCα synergistically potentiated the
vasorelaxant effect of RhoA/ROCK inhibition. Conclusion: The present study provides the first
evidence that RhoA activity is downregulated by PKCα in depolarized and PDBu treated freshly
isolated VSMCs and arteries, with an important physiological role on arterial contractility. | es |
dc.format | application/pdf | es |
dc.format.extent | 18 p. | es |
dc.language.iso | eng | es |
dc.relation.ispartof | Cellular Physiology And Biochemistry, 52 (1), 76-93. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Protein kinase C (PKC) | es |
dc.subject | Rho (Rho GTPase) | es |
dc.subject | Vascular smooth muscle cells | es |
dc.subject | Calcium channel | es |
dc.subject | Cell signaling | es |
dc.subject | Phorbol ester | es |
dc.subject | Depolarization | es |
dc.title | PKCα-Mediated Downregulation of RhoA Activity in Depolarized Vascular Smooth Muscle: Synergistic Vasorelaxant Effect of PKCα and ROCK Inhibition | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.contributor.sponsorship | This work was supported by the “Red de Investigación Cardiovascular, RIC,
RD12/0042/0041” of the Instituto de Salud Carlos III and by Ministerio de Economía y
Competitividad and FEDER (SAF2013-46806-R and SAF2017-89474-R) | |
dc.identifier.doi | 10.33594/000000006 | es |
dc.journaltitle | Cellular Physiology And Biochemistry | es |
dc.publication.volumen | 52 | es |
dc.publication.issue | 1 | es |
dc.publication.initialPage | 76 | es |
dc.publication.endPage | 93 | es |