Genetic polymorphisms of the ROMO1 intronic regions are not associated with the development of knee osteoarthritis

Authors

  • Claudia Frida Blancas-Meza Departamento de Biología, Facultad de Química. Universidad Nacional Autónoma de México (UNAM). Ciudad de México, México.
  • Gabriela Martínez-Nava Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Alberto López-Reyes Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Yessica Zamudio-Cuevas Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Karina Martínez-Flores Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Denise Clavijo-Cornejo Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Roxana Miranda-Labra Laboratorio de Fisiología Celular, Departamento de Ciencias de la Salud. Universidad Autónoma Metropolitana-Iztapalapa (UAM-I). Ciudad de México, México.
  • María Concepción Gutiérrez-Ruíz Laboratorio de Fisiología Celular, Departamento de Ciencias de la Salud. Universidad Autónoma Metropolitana-Iztapalapa (UAM-I). Ciudad de México, México.
  • Luis Enrique Gómez-Quiroz Laboratorio de Fisiología Celular, Departamento de Ciencias de la Salud. Universidad Autónoma Metropolitana-Iztapalapa (UAM-I). Ciudad de México, México.
  • Carlos Pineda Dirección de Investigación. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.
  • Javier Fernández-Torres Laboratorio de Líquido Sinovial. Instituto Nacional de Rehabilitación «Luis Guillermo Ibarra Ibarra». Ciudad de México, México.

Keywords:

Osteoarthritis, reactive oxygen species modulator 1, ROMO1 gene, single nucleotide polymorphisms, oxidative stress

Abstract

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.

Published

2024-08-19

How to Cite

1.
Blancas-Meza CF, Martínez-Nava G, López-Reyes A, Zamudio-Cuevas Y, Martínez-Flores K, Clavijo-Cornejo D, et al. Genetic polymorphisms of the ROMO1 intronic regions are not associated with the development of knee osteoarthritis. InDiscap [Internet]. 2024 Aug. 19 [cited 2024 Nov. 14];5(3):139-45. Available from: https://dsm.inr.gob.mx/indiscap/index.php/INDISCAP/article/view/343

Issue

Section

Original articles

Most read articles by the same author(s)

1 2 > >> 

Similar Articles

<< < 1 2 3 

You may also start an advanced similarity search for this article.