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Artículo

Focal adhesion kinase, RhoA, and p38 mitogen-activated protein kinase modulates apoptosis mediated by angiotensin II AT2 receptors

Manzur, Maria JimenaIcon ; Aguilera, Milton OsmarIcon ; Kotler, Monica LidiaIcon ; Beron, WalterIcon ; Ciuffo, Gladys MariaIcon
Fecha de publicación: 02/2019
Editorial: Wiley-liss, Div John Wiley & Sons Inc
Revista: Journal of Cellular Biochemistry
ISSN: 0730-2312
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Bioquímica y Biología Molecular

Resumen

Apoptosis plays an important role in cellular processes such as development, differentiation, and homeostasis. Although the participation of angiotensin II (Ang II) AT2 receptors (AT 2R) in cellular apoptosis is well accepted, the signaling pathway involved in this process is not well established. We evaluated the participation of signaling proteins focal adhesion kinase (FAK), RhoA, and p38 mitogen-activated protein kinase (p38MAPK) in apoptosis induced by Ang II via AT 2R overexpressed in HeLa cells. Following a short stimulation time (120 to 240 minutes) with Ang II, HeLa-AT 2 cells showed nuclear condensation, stress fibers disassembly and membrane blebbing. FAK, classically involved in cytoskeleton reorganization, has been postulated as an early marker of cellular apoptosis. Thus, we evaluated FAK cleavage, detected at early stimulation times (15 to 30 minutes). Apoptosis was confirmed by increased caspase-3 cleavage and enzymatic activity of caspase-3/7. Participation of RhoA was evaluated. HeLa-AT 2 cells overexpressing RhoA wild-type (WT) or their mutants, RhoA V14 (constitutively active form) or RhoA N19 (dominant-negative form) were used to explore RhoA participation. HeLa-AT 2 cells expressing the constitutively active variant RhoA V14 showed enhanced apoptotic features at earlier times as compared with cells expressing the WT variant. RhoA N19 expression prevented nuclear condensation/caspase activation. Inhibition of p38MAPK caused an increase in nuclear condensation and caspase-3/7 activation, suggesting a protective role of p38MAPK. Our results clearly demonstrated that stimulation of AT 2R induce apoptosis with participation of FAK and RhoA while p38MAPK seems to play a prosurvival role.
Palabras clave: ANGIOTENSIN II RECEPTORS , APOPTOTIC FEATURES , CASPASE ACTIVATION , FOCAL ADHESION KINASE , RHOA/RHO-ASSOCIATED KINASE
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/92604
DOI: http://dx.doi.org/10.1002/jcb.27496
URL: https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.27496
Colecciones
Articulos(IHEM)
Articulos de INST. HISTOLOGIA Y EMBRIOLOGIA DE MEND DR.M.BURGOS
Articulos(IMIBIO-SL)
Articulos de INST. MULTIDICIPLINARIO DE INV. BIO. DE SAN LUIS
Articulos(IQUIBICEN)
Articulos de INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CS. EXACTAS Y NATURALES
Citación
Manzur, Maria Jimena; Aguilera, Milton Osmar; Kotler, Monica Lidia; Beron, Walter; Ciuffo, Gladys Maria; Focal adhesion kinase, RhoA, and p38 mitogen-activated protein kinase modulates apoptosis mediated by angiotensin II AT2 receptors; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 120; 2; 2-2019; 1835-1849
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