Contribution of polymorphism in codon 72 of p53 gene to systemic lupus erythematosus in Poland

被引:12
作者
Piotrowski, P. [1 ]
Lianeri, M. [1 ]
Mostowska, M. [1 ]
Wudarski, M. [2 ]
Chwalinska-Sadowska, H. [2 ]
Jagodzinski, P. P. [1 ]
机构
[1] Karol Marcinkowski Univ Med Sci, Dept Biochem & Mol Biol, PL-60781 Poznan, Poland
[2] Inst Rheumatol, Warsaw, Poland
关键词
p53; gene; polymorphism; systemic lupus erythematosus;
D O I
10.1177/0961203307084722
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The contribution of the p53 Arg72Pro polymorphism in the development of systemic lupus erythematosus (SLE) remains controversial. We investigated the frequency of the p53 Arg72Pro Genotype in patients with SLE (n = 155) and in controls (n = 150) in Poland. We found a weak contribution of the Arg/Arg genotype to the morbidity of SLE. Odds ratio (OR) for patients with SLE and p53 Ara/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Ara/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328. Since the p53Arg variant supports apoptosis better than the p53Pro variant, our findings can be linked to an increase in the number of apoptotic leucocytes in SLE patients. The distinction between various populations may be because of differences in racial composition and/or exposure to distinct environmental factors that have a different impact on SLE incidence along with the changed Argp53Pro genotype.
引用
收藏
页码:148 / 151
页数:4
相关论文
共 31 条
[1]   Overexpression of the antiapoptotic gene Bfl-1 in B cells from patients with familial systemic lupus erythematosus [J].
Andre, J-M ;
Cimaz, R. ;
Ranchin, B. ;
Galambrun, C. ;
Bertrand, Y. ;
Rieux-Laucat, F. ;
Trescol-Biemont, M-C ;
Cochat, P. ;
Bonnefoy-Berard, N. .
LUPUS, 2007, 16 (02) :95-100
[2]   DERIVATION OF THE SLEDAI - A DISEASE-ACTIVITY INDEX FOR LUPUS PATIENTS [J].
BOMBARDIER, C ;
GLADMAN, DD ;
UROWITZ, MB ;
CARON, D ;
CHANG, CH .
ARTHRITIS AND RHEUMATISM, 1992, 35 (06) :630-640
[3]  
Chae BS, 2007, ARCH PHARM RES, V30, P191
[4]   Over-expression of TATA binding protein (TBP) and p53 and autoantibodies to these antigens are features of systemic sclerosis, systemic lupus erythematosus and overlap syndromes [J].
Chauhan, R ;
Handa, R ;
Das, TP ;
Pati, U .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2004, 136 (03) :574-584
[5]   The T cell enigma in lupus [J].
Dayal, AK ;
Kammer, GM .
ARTHRITIS AND RHEUMATISM, 1996, 39 (01) :23-33
[6]   AUTOANTIBODIES TO THE PROTEIN CORE OF VASCULAR BASEMENT-MEMBRANE HEPARAN-SULFATE PROTEOGLYCAN IN SYSTEMIC LUPUS-ERYTHEMATOSUS [J].
FILLIT, H ;
SHIBATA, S ;
SASAKI, T ;
SPIERA, H ;
KERR, LD ;
BLAKE, M .
AUTOIMMUNITY, 1993, 14 (03) :243-249
[7]  
HEPBURN AL, ANN RHEUM DIS
[8]   Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus [J].
Hochberg, MC .
ARTHRITIS AND RHEUMATISM, 1997, 40 (09) :1725-1725
[9]   HIGHER LUNG-CANCER RISK FOR YOUNGER AFRICAN-AMERICANS WITH THE PRO/PRO P53 GENOTYPE [J].
JIN, XM ;
WU, XF ;
ROTH, JA ;
AMOS, CI ;
KING, TM ;
BRANCH, C ;
HONN, SE ;
SPITZ, MR .
CARCINOGENESIS, 1995, 16 (09) :2205-2208
[10]   Systemic lupus erythematosus [J].
Kotzin, BL .
CELL, 1996, 85 (03) :303-306