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J Proteomics. 2014 Jun 25;106:246-59. doi: 10.1016/j.jprot.2014.04.036. Epub 2014 Apr 30.

Targets of protein carbonylation in spontaneously hypertensive obese Koletsky rats and healthy Wistar counterparts: a potential role on metabolic disorders.

Author information

  • 1Instituto de Investigaciones Marinas (IIM-CSIC), Eduardo Cabello 6, E-36208 Vigo, Spain.
  • 2Instituto de Investigaciones Marinas (IIM-CSIC), Eduardo Cabello 6, E-36208 Vigo, Spain. Electronic address: mpazos@iim.csic.es.
  • 3Unidad de Farmacología, Facultad de Medicina y Ciencias de la Salud, Universidad Rovira i Virgili, Sant Llorenç 21, E-43201 Reus, Spain.
  • 4Instituto de Química Avanzada de Catalunya (IQAC-CSIC), Jordi Girona 18-26, E-08034 Barcelona, Spain.

Abstract

The study innovatively pinpoints target proteins of carbonylation, a key PTM induced by oxidative stress, in the SHROB (genetically obese spontaneously hypertensive) rat model of metabolic syndrome (MetS). Protein carbonylation was assessed by a fluorescence-labeling proteomics approach, and complemented with biometric and biochemical markers of MetS. SHROB and healthy Wistar rats were fed two diets, soybean and linseed oil supplementations, in order to distinguish intrinsic carbonylation of SHROB animals from diet-modulated carbonylation unrelated to MetS. First exploratory data showed similar carbonylation patterns and metabolic conditions in SHROB rats fed soybean and linseed, but different from Wistar animals. A total of 18 carbonylated spots in liver, and 12 in skeletal tissue, related to pathways of lipid (29.6%), carbohydrate (25.9%) and amino acid (18.5%) metabolisms, were identified. In particular, SHROB animals present higher carbonylation in four liver proteins belonging to lipid metabolism, redox regulation and chaperone activity (ALDH2, PDI, PDIA3, PECR), and in the skeletal muscle ALDOA that is involved in muscle dysfunction. Conversely, SHROB rats display lower carbonylation in liver albumin, AKR1C9, ADH1 and catalase. This investigation provides a novel perspective of carbonylation in the context of metabolic disorders, and may be a starting point to characterize new redox pathways exacerbating MetS.

BIOLOGICAL SIGNIFICANCE:

Oxidative stress is a concomitant factor in the pathogenesis of MetS that induces oxidative PTM as carbonylation. Through the use of a redox proteomics approach, we have thoroughly mapped the occurrence of protein targets of carbonylation in the genetically-induced MetS model SHROB rat. The present research brings a new insight of MetS pathogenesis and it may provide valuable information to understand the biological impact of oxidative stress in patients with MetS.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

Metabolic syndrome; Oxidative stress; Protein carbonylation; Redox proteomics; SHROB model; Wistar rat

PMID:
24793432
[PubMed - indexed for MEDLINE]
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