Gene Expression Profiles of Peripheral Blood in a Family with Systemic Lupus Erythematosus
- VernacularTitle:系统性红斑狼疮患者及其家庭成员外周血基因表达谱的研究
- Author:
Guangming HAN
;
Shunle CHEN
;
Nan SHEN
;
Jing HUA
;
Yuan WANG
;
Chunde BAO
- Publication Type:Journal Article
- Keywords:
Lupus erythematosus, systemic;
Oligonucleotide sequence analysis;
Gene expression profiling
- From:
Chinese Journal of Dermatology
1995;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the pathogenesis of familial systemic lupus erythematosus (SLE), by analyzing the gene expression profile of peripheral blood in a family with 2 SLE patients and their first-degree relatives. Methods Total RNA was extracted from peripheral blood cells of normal subjects and SLE patients. Then, synthesis double strand cDNA template from total RNA, transcription of cRNA probe with Biotin labeling, hybridization of probe with Microarray, binding of Streptavidin to Biotin, amplification with First Antibody, further amplification with Cy3-Conjugated Second Antibody, detection of Cy3 dye with ScanArray 5000 were performed. With QuantArray microarray analysis software, the scan image information was converted into numeric data. With GeneSpring microarray analysis software, cluster analysis was done to find interested genes. Results Over 3000 target genes were analysed. Fifty-nine genes differentially expressed in familial SLE patients and controls were identified. Among them, 34 genes were up-regulated and 25 genes were down-regulated. These differentially expressed genes identified in two familial SLE patients were almost identical to those found in other sporadic SLE patients. Among 34 expression increasing genes, 22 were up-regulated in SLE sisters and unaffected sisters; among 25 expression decreased genes, 17 genes down-regulated in SLE sisters and unaffected sister. Cluster analysis showed that patients were clearly separated from controls and their unaffected sisters based on their gene expression profile. These results showed that in familial SLE, multiple genes were responsible for susceptibility to SLE, and clinically unaffected relatives shared some lupus susceptibility genes with their clinically affected relatives, in addition environmental factors were probably necessary to trigger disease. Conclusion These results indicate that high-density oligonucleotide microarray has the potential to explore the heredity in SLE families.
