RT Journal Article
T1 Klotho Prevents NFκB Translocation and Protects Endothelial Cell From Senescence Induced by Uremia
A1 Buendía, Paula
A1 Carracedo Añón, Julia María
A1 Soriano, Sagrario
A1 Madueño, Juan Antonio
A1 Ortiz, Alberto
A1 Martín Malo, Alejandro
A1 Aljama, Pedro
A1 Ramírez, Rafael
AB In patients with renal disease, uremia raises oxidative stress and senescence in endothelial cells, which can lead to endothelial dysfunction and cardiovascular disease. Klotho protein is a β-glucuronidase capable of hydrolyzing steroid β-glucuronides. This protein is recognized as an antiaging gene, that modulate both stress-induced senescence and functional response. The aim of the study was to investigate how senescence and oxidative stress induced by uremia in endothelial cells affects Klotho expression and whether intra or extracellular Klotho has effects on the response of these cells. Senescence and oxidative stress was obtained by exposure to uremic serum. Telomere length, the enzyme β-galactosidase, and oxidative stress were studied by flow cytometry. Nuclear factor kappa B activity was determined by electrophoretic mobility shift assay. The expression of Klotho decreased with the uremia and preceded the manifestations of cell aging. Levels of intracellular Klotho decreases associated to endothelial senescence, and exogenous Klotho prevents cellular senescence by inhibiting the increase in oxidative stress induced by uremia and diminished the nuclear factor kappa B–DNA binding ability.
PB Oxford University Press
SN 1079-5006
YR 2014
FD 2014-09-22
LK https://hdl.handle.net/20.500.14352/131627
UL https://hdl.handle.net/20.500.14352/131627
LA eng
NO Buendía, P., Carracedo, J., Soriano, S., Madueño, J. A., Ortiz, A., Martín-Malo, A., Aljama, P., & Ramírez, R. (2015). Klotho Prevents NFκB Translocation and Protects Endothelial Cell from Senescence Induced by Uremia. Journals of Gerontology - Series A Biological Sciences and Medical Sciences, 70(10), 1198-1209. https://doi.org/10.1093/GERONA/GLU170
NO This study was supported by grants from Fondo de Investigación Sanitaria, Instituto de Salud Carlos III (PI08/1038, PI09/00836, PI11/01536, PI12/01489) and Junta de Andalucía (JA0235/2009, JA0797-2010, P08-CTS-3797, P010-CTS-6337, P11-CTS-7352, RD12/0021/0011). P.B. was supported by a contract (Proyecto de Excelencia, Junta de Andalucía) from Fundación de Investigaciones Biomédicas de Córdoba (FIBICO). J.C.was supported by a contract from FIBICO (Programa Nicolas Monardes, Junta de Andalucía).
NO Instituto de Salud Carlos III
NO Junta de Andalucía
NO Fundación de Investigaciones Biomédicas de Córdoba
DS Docta Complutense
RD 19 mar 2026