Los polimorfismos LGALS3 + 191A y + 292C están asociados con una reducción en los niveles séricos de gal-3, pero no con los eventos clínicos de individuos con anemia falciforme

Autores/as

DOI:

https://doi.org/10.33448/rsd-v9i9.7314

Palabras clave:

Galectin-3; LGALS3; Polimorfismo; Anemia falciforme.

Resumen

Objetivo: Este estudio tuvo como objetivo evaluar si los polimorfismos de un solo nucleótido (SNPs) +191 C>A (rs4644) y +292 A>C (rs4652) del gen LGALS3 y los niveles séricos de galectina-3 (gal-3) están asociados con los eventos clínicos de pacientes con anemia falciforme (AF). Métodos: SNPs +191 y +292 en LGALS3 se estudiaron utilizando el sistema de PCR en tiempo real TaqMan; Los niveles séricos de gal-3 se midieron por ELISA. El estudio incluyó a 322 pacientes con AF, edad media 36 (21-84). Resultados: los genotipos AA y CA de la región +191 se relacionaron con niveles más bajos de gal-3 en comparación con el genotipo CC (p = 0.0296). El nivel más bajo de gal-3 también se asoció con los diplotipos + 191 / + 292 (AA / CC; CA / CC) (p = 0.0137) en comparación con los diplotipos (CC/AA; CC/CC; CC/AC; CA/CA). No hubo asociación entre los niveles séricos de galectina-3 y las frecuencias de genotipo de los polimorfismos LGALS3 +191 y +292 con eventos clínicos en SCA. Conclusión: Los polimorfismos +191 y +292 de LGALS3 están asociados con una disminución en los niveles séricos de gal-3. Sin embargo, no se observó asociación de polimorfismos y niveles séricos de gal-3 con eventos clínicos en pacientes con AF.

Citas

Abd El-Kader, S. M., & Al-Shreef, F. M. (2018). Impact of aerobic exercises on selected inflammatory markers and immune system response among patients with sickle cell anemia in asymptomatic steady state. Afr Health Sci, 18(1), 111-119.

Aciksari, G., Uygun, T., Atici, A., et al. (2020) Association between galectin-3 levels and isolated coronary artery ectasia.Cardiovasc J Afr, 5(31), 1-6.

Atabaki, M., Hashemi, M., Daneshvar, H., Alijani, E. (2017). Lectin, galactoside binding, soluble, 3 rs4652 A/C gene variation andthe risk for rheumatoid arthritis. Biomed Rep. 6(2),251-255.

Bartolucci, P., Brugnara, C., Teixeira-Pinto, A., et al. (2012) Erythrocyte density in sickle cell syndromes is associated with specific clinical manifestations and hemolysis. Blood, 120, 3136-3141.

Chen, S. S., Sun, L. W., Brickner, H., & Sun, P. Q. (2015). Downregulating galectin-3 inhibits proinflammatory cytokine production by human monocyte-derived dendritic cells via RNA interference. Cell Immunol, 294, 44-53.

Cruz, C. S., Angelo, A. L. D., Larocca, T. F., et al. (2015) Avaliação do polimorfismo da galectina-3 em indivíduos com doença de chagas crônica. Arq bras cardiol, 21, 185-192.

Davis, L. G., Dibner, M. D., & Battey, J. F. (1986). Basic method in molecular biology. Londres: Elservier, 338-388.

De Carvalho-Siqueira, G. Q., Ananina, G., de Souza, B. B., et al. (2019). Whole-exome sequencing indicates FLG2 variant associated with leg ulcers in Brazilian sickle cell anemia patients. Exp Biol Med(Maywood), 1-8.

Domingos, I. F., Pereira-Martins, D. A., Sobreira, M. J. V. C., et al. (2020). High levels of proinflammatory cytokines IL-6 and IL-8 are associated with a poor clinical outcome in sickle cell anemia. Ann Hematol, 99(5), 947-953.

Feng, W., Wu, X., Li, S., et al. (2017). Association of serum galectin-3 with the acute exacerbation of chronic obstructive pulmonary disease. Med Sci Monit, 26(23), 4612-4618.

George, M., Shammugam, E., Srivatsan, V., et al. (2015). value of pentraxin-3 and galectin-3 in acute coronary syndrome: a short-term prospective cohort study.Ther Adv Cardiovasc Dis, 5, 275-284.

Higgs, D. R., & Wood, W. G. (2008). Genetic complexity in sickle cell disease. Proc Natl Acad Sci USA, 105(33), 11595-11596.

Hu, C. Y., Chang, S. K., Wu, C. S., Tsai, W. I., Hsu, P. N.. (2011). Galectin-3 gene (LGALS3) +292C allele is a geneticpredisposition factor for rheumatoid arthritis in Taiwan. Clin Rheumatol, 30,1227-1233.

Huttle, A., Maestre, G. E., Lantigua, R., & Green, N. S. (2015). Sckle cell in sckle cell disease in Latin America e the United States. Pediatr blood Cancer, 62, 1131-1136.

Jorgensen, D. R., Rosano, C., & Novelli, E. M. (2016). Can Neuroimaging Markers of Vascular Pathology Explain Cognitive Performance in Adults With Sickle Cell Anemia? A review of the Literature. Hemoglobin, 40(6),381-387.

Kosaraju, V., Harwani, A., Partovi, S., et al. (2017). Imaging of musculoskeletal manifestations in sickle cell disease patients. Br J Radiol, 90(1073):20160130.

Marques, V., Souza, R. A. P. R., Ramos, L. J., Zan, R. A., Meneguetti, D. U. O. (2012). Revendo a anemia falciforme: Sintomas, tratamento e perspectivas.Rev Cie Fac Edu Mei Amb, 3(1),39-61.

Mendonça-Belmont, T. F., Do, Ó. K. P., Soares Silva, A., et al. (2016). Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 gene (LGALS3) related to lower GAL-3 serum levels are associated with frequant respiratory tract infection and vaso-oclusive crisis in children with sickle cell anemia. Plos One, 11(9).

Minniti, C. P., Eckman, J., Sebastiani, P., Steinberg, M. H., & Bellas, S. K. (2010). Leg ulcers in sickle cell disease. Am J Hematol, 85(10), 831-833.

Minniti, C. P., & Kato, G. J. (2016). Critical reviews: how we treat sickle cell patients with leg ulcers.Am J Hematol, 91, 22-30.

Numano, F., Shimizu, C., Jimenez-Fernandez, S., et al. (2015). Galectin-3 is a marker of myocardial and vascular fibrosis in kwasaki disease patients with giant aneurysms. International jornal. Of cardiology, 201, 429-437.

Parker, D. M., Owens, S. L., Ramkumar, N., et al. (2019). Galectin-3 as a predictor of long-term survival after isolated coronary artery bypass grafting surgery. Ann Thorac Surg.

Pitanga, T. N., Oliveira, R. R., Zanette, D. L., et al. (2016). Sickle red cells as danger signals on proinflammatory gene expression, leukotriene B4 and interleukin-1 beta production in peripheral blood mononuclear cell. Cytokine, 83, 75‐84.

Rabinovich, G. A., Baum, L. G., Tinari, N., et al. (2002). Galectins and their ligands: amplifiers, silencersnor tuners of the inflammatory response? TRENDS in immunology, 23(6), 313-320.

Rebholz, C. M., Selvin, E., Liang, M., Ballantyne, C. M., Hoogeveen, R. C., Aguilar, D. (2018). Plasma galectin-3 levels are associated with the risk of incident chronic kidney disease.Kidney Int, 93(1):252-259.

Rêgo, M. J., da Silva, R. R., Pereira, M. C., et al. (2015). Evaluation of CD4(+) CD25(+) FoxP3(+) T cell populations, IL-10 production, and their correlation with clinical and biochemical parameters in sickle cell anemia patients with leg ulcers. Cytokine. 75(2),310-315.

Romaniuk, M. A., Negrotto, S., Campetella, O., Rabinovich, G. A., Schattner, M. (2011). identification of galectins as novel regulators of platelet signaling and function. IUBMB Life, 63(7),521-527.

Sanchaisuriya, K., Chunpanich, S., Fucharoen, G., & Fucharoen, S. (2004). Multiplex allelespecific PCR assay for differential diagnosis of Hb S, Hb D-Punjab and Hb Tak. Clin. Chim. Acta, 343 129–34.

Senet, P., Blas-Chatelain, C., Levy, P., et al. (2017). Factors predictive of leg-ulcer healing in sickle cell disease: a multicentre, prospective cohort study. Br J Dermatol, 177(1),206-211.

Serjeant, G. R. Understating the morbidity of sickle cell disease. (1997). British Journal of Haematology, 99(4), 976-977.

Shen, Q., Chen, W., Liu, J., & Liang, Q. (2019). Galectin-3 aggravates pulmonary arterial hypertension via immunomodulation in congenital heart disease. Life Sci, 1(232).

Wagdy, R., Suliman, H., Bamashmose, B., et al. (2018). Subclinical myocardial injury during vaso-occlusive crisis in pediatric sickle cell disease.Eur J Pediatr, 177(12), 1745-1752.

Wang, A., Zhong, C., Zhu, Z., et al. (2018). Serum Galectin-3 and poor outcomes among patients with acute ischemic stroke. Stroke, 49(1), 211-214.

Zhang, Y., Wang, Y., Zhai, M., et al. (2018). Influence of LGALS3 gene polymorphisms on susceptibility and prognosis of dilated cardiomyopathy in a Northern Han Chinese population. Gene. 5(642), 293-298.

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Publicado

23/08/2020

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Ó, K. P. do; MENDONÇA-BELMONT, T. F. de .; FARIAS, I. C. C.; SILVA, A. S. da .; FREIRE, A. K. da S. .; MOURA, P. M. M. F. de .; VASCONCELOS, L. R. S. .; ARAÚJO, A. da S. .; ARCANJO, G. da S. .; FALCÃO, D. A. .; HATZLHOFER, B. L. D. .; LUCENA-ARAÚJO , A. R. . .; BEZERRA, M. A. C. .; CAVALCANTI, M. do S. de M. . Los polimorfismos LGALS3 + 191A y + 292C están asociados con una reducción en los niveles séricos de gal-3, pero no con los eventos clínicos de individuos con anemia falciforme. Research, Society and Development, [S. l.], v. 9, n. 9, p. e442997314, 2020. DOI: 10.33448/rsd-v9i9.7314. Disponível em: https://rsdjournal.org/index.php/rsd/article/view/7314. Acesso em: 27 sep. 2024.

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Ciencias de la salud