Genetic polymorphisms of the ROMO1 intronic regions are not associated with the development of knee osteoarthritis
Keywords:
Osteoarthritis, reactive oxygen species modulator 1, ROMO1 gene, single nucleotide polymorphisms, oxidative stressAbstract
Osteoarthritis (OA) is a degenerative disorder that is characterized by articular cartilage break-
down, osteophytes formation, and subchondral bone sclerosis; its development and progression
are mediated by proinflammatory mediators, as well as by reactive oxidative species (ROS).
Recently there has been identified a mitochondrial protein called Romo1 that modulates ROS
in different states of oxidative stress, and which is encoded by the gene ROMO1. This gene
has single nucleotide polymorphisms (SNPs) that could affect the translation of the different
isoforms of its associated protein, and it is unknown whether these could have implications in the modulation of ROS in patients with OA. The aim of this work was evaluate two polymor- phisms of ROMO1 gene in samples of patients with knee OA. We found that the analyzed polymorphisms are not associated with the presence of OA, therefore are not useful markers for genetic studies of OA in Mexican population.
References
Meulenbelt I. Osteoarthritis year 2011 in review: genet- ics. Osteoarthritis Cartilage. 2012; 20 (3): 218-222.
Arden N, Nevitt MC. Osteoarthritis: epidemiology. Best Pract Res Clin Rheumatol. 2006; 20 (1): 3-25.
De Filippis L, Gulli S, Caliri A, Romano C, Munaò F, Trimarchi G et al. Epidemiology and risk factors in os- teoarthritis: literature review data from “OASIS” study. Reumatismo. 2004; 56 (3): 169-184.
Peláez-Ballestas I, Sanin LH, Moreno-Montoya J, Alvarez-Nemegyei J, Burgos-Vargas R, Garza-Elizondo M et al. Epidemiology of the rheumatic diseases in Mexico. A study of 5 regions based on the COPCORD methodology. J Rheumatol Suppl. 2011; 86: 3-8.
Woolf AD, Pfleger B. Burden of major musculoskeletal conditions. Bull World Health Organ. 2003; 81 (9): 646-656. 6. Fernández-Moreno M, Rego I, Blanco FJ. Genetics in osteoarthritis Reumatol Clin. 2007; 3 Suppl 3: S13-S18. 7. Chapman K, Valdes AM. Genetic factors in OA patho-
genesis. Bone. 2012; 51 (2): 258-264.
Akkiraju H, Nohe A. Role of chondrocytes in cartilage
formation, progression of osteoarthritis and cartilage
regeneration. J Dev Biol. 2015; 3 (4): 177-192.
Atik OŞ, Erdoğan D, Seymen CM, Bozkurt HH, Kaplanoğlu GT. Is there crosstalk between subchondral bone, carti- lage, and meniscus in the pathogenesis of osteoarthritis?
Eklem Hastalik Cerrahisi 2016; 27 (2): 62-67.
FengX,ShiY,XuL,PengQ,WangF,WangXetal. Modulation of IL-6 induced RANKL expression in arthritic synovium by a transcription factor SOX5. Sci Rep. 2016;
: 32001. doi: 10.1038/srep32001.
RasheedN,AlghashamA,RasheedZ.Lactoferrinfrom
camelus dromedarius inhibits nuclear transcription factor- kappa B activation, cyclooxygenase-2 expression and prostaglandin E2 production in stimulated human chon- drocytes. Pharmacognosy Res. 2016; 8 (2): 135-141.
Pérez-GarcíaS,CarriónM,Gutiérrez-CañasI,González- Álvaro I, Gomariz RP, Juarranz Y. VIP and CRF reduce ADAMTS expression and function in osteoarthritis syno- vial fibroblasts. J Cell Mol Med. 2016; 20 (4): 678-687.
Utomo L, Bastiaansen-Jenniskens YM, Verhaar JA,
van Osch GJ. Cartilage inflammation and degeneration
is enhanced by pro-inflammatory (M1) macrophages
in vitro, but not inhibited directly by anti-inflammatory
(M2) macrophages. Osteoarthritis Cartilage 2016 Aug 5. pii: S1063-4584(16)30209-6. doi: 10.1016/j. joca.2016.07.018.
Ziskoven C, Jäger M, Zilkens C, Bloch W, Brixius K, Krauspe R. Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation? Orthop Rev (Pavia). 2010; 2 (2): e23. doi: 10.4081/or.2010.e23.
Poulet B, Beier F. Targeting oxidative stress to reduce osteoarthritis. Arthritis Res Ther. 2016; 18: 32. doi: 10.1186/s13075-015-0908-7.
Chevalier X, Eymard F, Richette P. Biologic agents in osteoarthritis: hopes and disappointments. Nat Rev Rheumatol. 2013; 9 (7): 400-410. doi: 10.1038/ nrrheum.2013.44.
Lepetsos P, Papavassiliou AG. ROS/oxidative stress signaling in osteoarthritis. Biochim Biophys Acta. 2016; 1862 (4): 576-591. doi: 10.1016/j.bbadis.2016.01.003.
De Biasi S, Gibellini L, Bianchini E, Nasi M, Pinti M, Salvioli S et al. Quantification of mitochondrial reactive oxygen species in living cells by using multi-laser poly- chromatic flow cytometry. Cytometry A. 2016 Aug 30. doi: 10.1002/cyto.a.22936.
Chung YM, Lee SB, Kim HJ, Park SH, Kim JJ, Chung JS et al. Replicative senescence induced by Romo1- derived reactive oxygen species. J Biol Chem. 2008; 283 (48): 33763-33771.
Chung YM, Kim JS, Yoo YD. A novel protein, Romo1, induces ROS production in the mitochondria. Biochem Biophys Res Commun. 2006; 347 (3): 649-655.
Chung JS, Lee SB, Park SH, Kang ST, Na AR, Chang TS et al. Mitochondrial reactive oxygen species originat- ing from Romo1 exert an important role in normal cell cycle progression by regulating p27(Kip1) expression. Free Radic Res. 2009; 43 (8): 729-737.
http://www.ncbi.nlm.nih.gov/gene/140823
Sherry ST, Ward MH, Kholodov M, Baker J, Phan L, Smigielski EM et al. dbSNP: the NCBI database of
genetic variation. Nucleic Acids Res. 2001; 29 (1):
-311.
Altman R, Asch E, Bloch D, Bole G, Borenstein D, Brandt
K et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the knee. Arthritis Rheum 1986; 29: 1039-1049.
http://browser.1000genomes.org/index.html
Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis. 1957; 16 (4): 494-502. 27. Wu H, Gu YH, Wei L, Guo TK, Zhao Y, Su G et al. As- sociation of Romo1 gene genetic polymorphisms with risk of gastric cancer in northwestern Chinese popula-
tion. Pathol Oncol Res. 2015; 21 (3): 581-587.
Petrovic MG, Kruzliak P, Petrovic D. The rs6060566 of the reactive oxygen species modulator 1 (Romo-1) gene affects Romo-1 expression and the development of diabetic retinopathy in Caucasians with type 2 diabetes. Acta Ophthalmol. 2015; 93 (8): e654-e657. doi: 10.1111/
aos.12723. Epub 2015 Mar 30.
Mazzetti I, Grigolo B, Pulsatelli L, Dolzani P, Silvestri
T, Meliconi R et al. Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis. Clin Sci. 2001; 101 (6): 593-599.
Henrotin YE, Bruckner P, Pujol JP. The role of reactive oxygen species in homeostasis and degradation of car- tilage. Osteoarthritis Cartilage 2003; 11 (10): 747-755.
Mathy-Hartert M, Martin G, Devel P, Deby-Dupont G, Pujol JP, Reginster JY et al. Reactive oxygen species downregu- late the expression of pro-inflammatory genes by human chondrocytes. Inflamm Res. 2003; 52 (3): 111-118.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2016 Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra
This work is licensed under a Creative Commons Attribution 4.0 International License.
© Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra under a Creative Commons Attribution 4.0 International (CC BY 4.0) license which allows to reproduce and modify the content if appropiate recognition to the original source is given.