Blockade of TGF-β 1 Signalling Inhibits Cardiac NADPH Oxidase Overactivity in Hypertensive Rats

NADPH oxidases constitute a major source of superoxide anion (·O(2) (-)) in hypertension. Several studies suggest an important role of NADPH oxidases in different effects mediated by TGF-β 1. In this study we show that chronic administration of P144, a peptide synthesized from type III TGF-β 1 recep...

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Authors: Miguel-Carrasco, J.L. (José Luis)|||/items/626cda34-5a0d-43e1-a34e-33d5f8c77fa6, Baltanas, A. (Ana)|||/items/480d0aa5-fd6e-4a33-a021-afb4e32b1861, Cebrian, C. (Carolina)|||/items/ac1a05ff-5b20-4d11-80ca-80c922e2acae, Moreno-Zulategui, M.U. (María de Ujue)|||/items/c970940e-b812-4c54-b9ee-26a5e0b78ec7, Lopez-Salazar, M.B. (María Begoña)|||/items/153e0e37-14b0-403e-afab-8af00c4edde0, Hermida, N. (Nerea)|||/items/4473dd6e-967a-481c-b1c7-e8914ba31b83, Gonzalez, A. (Arantxa)|||/items/9c64c0f4-66b4-4b51-8593-0e50c091a515, Dotor, J. (Javier)|||/items/6606b7a3-73b7-49d9-bc1b-c565b3e1c208, Borras-Cuesta, F. (Francisco)|||/items/9f3719bd-4cf6-4e5b-b672-39179b54e8cc, Diez-Martinez, J. (Javier)|||/items/4f3a0e43-12bf-403d-9dc7-31fab0d11d41, Fortuño, A. (Ana)|||/items/2324831f-71b3-4d1b-afc1-594e4e1bc0c9, Zalba-Goñi, G. (Guillermo)|||/items/71410fa2-baa5-4efc-bce7-14b4b0e23802
Format: article
Publication Date:2012
Country:España
Institution:Universidad de Navarra
Repository:Dadun. Depósito Académico Digital de la Universidad de Navarra
Language:English
OAI Identifier:oai:dadun.unav.edu:10171/22822
Online Access:https://hdl.handle.net/10171/22822
Access Level:Open access
Keyword:Cardiac NADPH oxidase
TGF-beta 1
Hypertensive rats
Description
Summary:NADPH oxidases constitute a major source of superoxide anion (·O(2) (-)) in hypertension. Several studies suggest an important role of NADPH oxidases in different effects mediated by TGF-β 1. In this study we show that chronic administration of P144, a peptide synthesized from type III TGF-β 1 receptor, significantly reduced the cardiac NADPH oxidase expression and activity as well as in the nitrotyrosine levels observed in control spontaneously hypertensive rats (V-SHR) to levels similar to control normotensive Wistar Kyoto rats. In addition, P144 was also able to reduce the significant increases in the expression of collagen type I protein and mRNA observed in hearts from V-SHR. In addition, positive correlations between collagen expression, NADPH oxidase activity, and nitrotyrosine levels were found in all animals. Finally, TGF-β 1-stimulated Rat-2 exhibited significant increases in NADPH oxidase activity that was inhibited in the presence of P144. It could be concluded that the blockade of TGF-β 1 with P144 inhibited cardiac NADPH oxidase in SHR, thus adding new data to elucidate the involvement of this enzyme in the profibrotic actions of TGF-β 1.

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