Patients with Systemic Sclerosis Present Increased DNA Damage Differentially Associated with DNA Repair Gene Polymorphisms
Carregando...
Citações na Scopus
21
Tipo de produção
article
Data de publicação
2014
Título da Revista
ISSN da Revista
Título do Volume
Editora
J RHEUMATOL PUBL CO
Autores
PALOMINO, Gustavo Martelli
BASSI, Carmen L.
WASTOWSKI, Isabela J.
XAVIER, Danilo J.
LUCISANO-VALIM, Yara M.
CRISPIM, Janaina C. O.
RASSI, Diane M.
SAKAMOTO-HOJO, Elza T.
MOREAU, Philippe
Citação
JOURNAL OF RHEUMATOLOGY, v.41, n.3, p.458-465, 2014
Resumo
Objective. Patients with systemic sclerosis (SSc) exhibit increased toxicity when exposed to genotoxic agents. In our study, we evaluated DNA damage and polymorphic sites in 2 DNA repair genes (XRCC1 Arg399Gln and XRCC4 Ile401Thr) in patients with SSc. Methods. A total of 177 patients were studied for DNA repair gene polymorphisms. Fifty-six of them were also evaluated for DNA damage in peripheral blood cells using the comet assay. Results. Compared to controls, the patients as a whole or stratified into major clinical variants (limited or diffuse skin involvement), irrespective of the underlying treatment schedule, exhibited increased DNA damage. XRCC1 (rs: 25487) and XRCC4 (rs: 28360135) allele and genotype frequencies observed in patients with SSc were not significantly different from those observed in controls; however, the XRCC1 Arg399Gln allele was associated with increased DNA damage only in healthy controls and the XRCC4 Ile401Thr allele was associated with increased DNA damage in both patients and controls. Further, the XRCC1 Arg399Gln allele was associated with the presence of antinuclear antibody and anticentromere antibody. No association was observed between these DNA repair gene polymorphic sites and clinical features of patients with SSc. Conclusion. These results corroborate the presence of genomic instability in SSc peripheral blood cells, as evaluated by increased DNA damage, and show that polymorphic sites of the XRCC1 and XRCC4 DNA repair genes may differentially influence DNA damage and the development of auto-antibodies.
Palavras-chave
SYSTEMIC SCLEROSIS, COMET ASSAY, DNA REPAIR, DNA DAMAGE, XRCC1 AND XRCC4
Referências
- Abdel-Rahman SZ, 2000, CANCER LETT, V159, P79, DOI 10.1016/S0304-3835(00)00537-1
- Abraham D, 2007, ARTHRITIS RES THER, V9, DOI 10.1186/ar2186
- Abraham DJ, 2005, TRENDS IMMUNOL, V26, P587, DOI 10.1016/j.it.2005.09.004
- Artlett CM, 1996, BRIT J RHEUMATOL, V35, P732
- Bassi CL, 2008, LUPUS, V17, P988, DOI 10.1177/0961203308093461
- Brem R, 2008, DNA REPAIR, V7, P849, DOI 10.1016/j.dnarep.2008.02.002
- Burma S, 2006, DNA REPAIR, V5, P1042, DOI 10.1016/j.dnarep.2006.05.026
- Burt RK, 2004, BONE MARROW TRANSPL, V34, P745, DOI 10.1038/sj.bmt.1704671
- Caldecott KW, 1996, NUCLEIC ACIDS RES, V24, P4387, DOI 10.1093/nar/24.22.4387
- Derk CT, 2007, CLIN RHEUMATOL, V26, P1615, DOI 10.1007/s10067-007-0546-9
- Domsic RT, 2011, NAT REV RHEUMATOL, V7, P628, DOI 10.1038/nrrheum.2011.152
- Duarte MC, 2005, WORLD J GASTROENTERO, V11, P6593
- Duell EJ, 2001, CANCER EPIDEM BIOMAR, V10, P217
- EILAT D, 1994, MOL IMMUNOL, V31, P1377, DOI 10.1016/0161-5890(94)90154-6
- Evans MD, 2006, GENOME DYN, V1, P53, DOI 10.1159/000092500
- FENECH M, 1993, MUTAT RES, V285, P35, DOI 10.1016/0027-5107(93)90049-L
- Fontana L, 2008, ANTICANCER RES, V28, P1853
- Ford BN, 2000, CARCINOGENESIS, V21, P1977, DOI 10.1093/carcin/21.11.1977
- Garg DK, 1998, J AUTOIMMUN, V11, P371, DOI 10.1006/jaut.1998.0208
- Genestier L, 1998, J CLIN INVEST, V102, P322, DOI 10.1172/JCI2676
- GOODE HF, 1993, CRIT CARE MED, V21, P1770, DOI 10.1097/00003246-199311000-00029
- Griswold WR, 1997, PEDIATR NEPHROL, V11, P699
- Grob M, 1998, J CUTAN PATHOL, V25, P275, DOI 10.1111/j.1600-0560.1998.tb01733.x
- HOUSSET E, 1969, CR ACAD SCI D NAT, V269, P413
- Kamanh A, 2004, CELL BIOCHEM FUNCT, V22, P53, DOI 10.1002/cbf.1055
- KERR LD, 1992, J RHEUMATOL, V19, P294
- Lee KJ, 2002, J IMMUNOL, V169, P3413
- Lees-Miller SP, 2003, BIOCHIMIE, V85, P1161, DOI 10.1016/j.biochi.2003.10.011
- Lei YC, 2002, MUTAT RES-GEN TOX EN, V519, P93, DOI 10.1016/S1383-5718(02)00127-4
- LEROY EC, 1988, J RHEUMATOL, V15, P202
- LIPSKY PE, 1984, J CLIN INVEST, V73, P53, DOI 10.1172/JCI111207
- Lo SF, 2012, RHEUMATOL INT, V32, P3723, DOI 10.1007/s00296-011-2185-3
- Majone F, 2006, EUR J DERMATOL, V16, P258
- Makker SP, 1996, PEDIATR NEPHROL, V10, P7
- Martins EP, 2010, SCAND J RHEUMATOL, V39, P398, DOI 10.3109/03009741003685640
- MASI A T, 1980, Arthritis and Rheumatism, V23, P581, DOI 10.1002/art.1780230510
- Masson M, 1998, MOL CELL BIOL, V18, P3563
- McConnell JR, 2002, CLIN EXP RHEUMATOL, V20, P653
- McCurdy D, 1997, RADIAT RES, V147, P48, DOI 10.2307/3579442
- Migliore L, 1999, MUTAGENESIS, V14, P227, DOI 10.1093/mutage/14.2.227
- MILLER SA, 1988, NUCLEIC ACIDS RES, V16, P1215, DOI 10.1093/nar/16.3.1215
- O'Donovan P, 2005, SCIENCE, V309, P1871, DOI 10.1126/science.1114233
- Porciello G, 2002, Reumatismo, V54, P36
- Porciello G, 2003, J RHEUMATOL, V30, P1244
- Porciello G, 2004, EUR J DERMATOL, V14, P327
- Relton CL, 2004, MUTAT RES-FUND MOL M, V545, P49, DOI 10.1016/j.mrfmmm.2003.09.007
- Sampaio-Barros PD, 2012, J RHEUMATOL, V39, P1971, DOI 10.3899/jrheum.111582
- Shen HB, 2000, INT J CANCER, V88, P601, DOI 10.1002/1097-0215(20001115)88:4<601::AID-IJC13>3.0.CO;2-C
- Simonini G, 1999, MOL CELL BIOCHEM, V196, P85, DOI 10.1023/A:1006922313774
- Sturgis EM, 1999, CARCINOGENESIS, V20, P2125, DOI 10.1093/carcin/20.11.2125
- Thompson LH, 2000, MUTAT RES-DNA REPAIR, V459, P1, DOI 10.1016/S0921-8777(99)00058-0
- Tsuruta D, 2013, EUR J DERMATOL, V23, P117, DOI 10.1684/ejd.2012.1902
- van Bon L, 2011, CURR OPIN RHEUMATOL, V23, P505, DOI 10.1097/BOR.0b013e32834b0dac
- Waris G, 2004, LIFE SCI, V75, P2633, DOI 10.1016/j.lfs.2004.04.034
- Wong RH, 2008, MUTAT RES-GEN TOX EN, V654, P168, DOI 10.1016/j.mrgentox.2008.06.005
- Yu CL, 1998, SCAND J RHEUMATOL, V27, P54
- Zhang HJ, 2011, ANTICANCER RES, V31, P3945
- Zhou W, 2003, CANCER EPIDEM BIOMAR, V12, P359