Protein Carbonylation in Patients with Myelodysplastic Syndrome: An Opportunity for Deferasirox Therapy.
Rodríguez-García A1, Morales ML2, Garrido-García V3, García-Baquero I4, Leivas A5, Carreño-Tarragona G6, Sánchez R7, Arenas A8, Cedena T9, Ayala RM10, Bautista JM11, Martínez-López J12,13, Linares M14,15.
Antioxidants (Basel). 2019 Oct 24;8(11). pii: E508. doi: 10.3390/antiox8110508.

Abstract
Control of oxidative stress in the bone marrow (BM) is key for maintaining the interplay between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such
as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an indicator of oxidative stress in the BM of patients with MDS and control subjects, and also patients
with MDS under treatment with the iron chelator deferasirox (DFX). As expected, differences in the pattern of protein carbonylation were observed in BM samples between MDS patients and controls, with an increase in protein carbonylation in the former.
Strikingly, patients under DFX treatment had lower levels of protein carbonylation in BM with respect to untreated patients. Proteomic analysis identified four proteins with high carbonylation levels in MDS BM cells. Finally, as oxidative stress-related
signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment.
Overall, our results suggest that the fine-tuning of oxidative stress levels in the BM of patients with MDS might control malignant progression.

KEYWORDS:
carbonylation; deferasirox; myelodysplastic syndromes; oxidative stress

PMID: 31652983 DOI: 10.3390/antiox8110508
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