| dc.contributor.author |
Oikonomidou, O |
en |
| dc.contributor.author |
Vlachoyiannopoulos, PG |
en |
| dc.contributor.author |
Kominakis, A |
en |
| dc.contributor.author |
Kalofoutis, A |
en |
| dc.contributor.author |
Moutsopoulos, HM |
en |
| dc.contributor.author |
Moutsatsou, P |
en |
| dc.date.accessioned |
2014-06-06T06:47:18Z |
|
| dc.date.available |
2014-06-06T06:47:18Z |
|
| dc.date.issued |
2006 |
en |
| dc.identifier.issn |
10217401 |
en |
| dc.identifier.uri |
http://dx.doi.org/10.1159/000100474 |
en |
| dc.identifier.uri |
http://62.217.125.90/xmlui/handle/123456789/3512 |
|
| dc.subject |
AP-1 |
en |
| dc.subject |
Autoimmunity |
en |
| dc.subject |
Glucocorticoid receptor |
en |
| dc.subject |
JNK |
en |
| dc.subject |
Lymphocytes |
en |
| dc.subject |
NFκB |
en |
| dc.subject |
Systemic lupus erythematosus |
en |
| dc.subject.other |
azathioprine |
en |
| dc.subject.other |
cell extract |
en |
| dc.subject.other |
cyclophosphamide |
en |
| dc.subject.other |
glucocorticoid receptor |
en |
| dc.subject.other |
hydroxychloroquine |
en |
| dc.subject.other |
immunoglobulin enhancer binding protein |
en |
| dc.subject.other |
mycophenolic acid 2 morpholinoethyl ester |
en |
| dc.subject.other |
prednisolone |
en |
| dc.subject.other |
protein antibody |
en |
| dc.subject.other |
protein c fos |
en |
| dc.subject.other |
receptor antibody |
en |
| dc.subject.other |
stress activated protein kinase 1 |
en |
| dc.subject.other |
synaptotagmin I |
en |
| dc.subject.other |
transcription factor AP 1 |
en |
| dc.subject.other |
adult |
en |
| dc.subject.other |
article |
en |
| dc.subject.other |
cell isolation |
en |
| dc.subject.other |
clinical article |
en |
| dc.subject.other |
controlled study |
en |
| dc.subject.other |
corticosteroid therapy |
en |
| dc.subject.other |
drug dose comparison |
en |
| dc.subject.other |
drug megadose |
en |
| dc.subject.other |
female |
en |
| dc.subject.other |
gel mobility shift assay |
en |
| dc.subject.other |
human |
en |
| dc.subject.other |
human cell |
en |
| dc.subject.other |
immunoblotting |
en |
| dc.subject.other |
low drug dose |
en |
| dc.subject.other |
peripheral lymphocyte |
en |
| dc.subject.other |
priority journal |
en |
| dc.subject.other |
protein DNA binding |
en |
| dc.subject.other |
systemic lupus erythematosus |
en |
| dc.subject.other |
treatment outcome |
en |
| dc.subject.other |
Adult |
en |
| dc.subject.other |
Blotting, Western |
en |
| dc.subject.other |
DNA |
en |
| dc.subject.other |
Electrophoretic Mobility Shift Assay |
en |
| dc.subject.other |
Female |
en |
| dc.subject.other |
Humans |
en |
| dc.subject.other |
Immunoblotting |
en |
| dc.subject.other |
JNK Mitogen-Activated Protein Kinases |
en |
| dc.subject.other |
Lupus Erythematosus, Systemic |
en |
| dc.subject.other |
Lymphocytes |
en |
| dc.subject.other |
Receptors, Glucocorticoid |
en |
| dc.subject.other |
Transcription Factor AP-1 |
en |
| dc.title |
Glucocorticoid receptor, nuclear factor κB, activator protein-1 and c-jun N-terminal kinase in systemic lupus erythematosus patients |
en |
| heal.type |
journalArticle |
en |
| heal.identifier.primary |
10.1159/000100474 |
en |
| heal.publicationDate |
2006 |
en |
| heal.abstract |
Objective: Due to the crucial role of the glucocorticoid receptor (GR), nuclear factor κB (NFκB), activator protein-1 (AP-1) and c-jun N-terminal kinase (JNK) in regulating inflammatory mediators and immune responses, we investigated their potential role in systemic lupus erythematosus (SLE). Patients and Methods: Whole cell and nuclear extracts from peripheral blood lymphocytes, isolated from 25 SLE patients and 25 controls, were immunoblotted using GR, p65/NFκB, c-fos and JNK1 antibodies. The electrophoretic mobility shift assay (EMSA) assessed GR, NFκB and AP-1-DNA binding in nuclear aliquots. Associations with the disease state and the doses of corticosteroids administered were studied. Results: (i) SLE patients had lower GR-DNA binding (p < 0.001), NFκB-DNA binding (p < 0.001) and whole cell c-fos (p < 0.01) but higher nuclear NFκB (p < 0.01). (ii) SLE patients and controls had similar AP-1-DNA binding, nuclear c-fos, GR and JNK, whole cell GR, NFκB and JNK. (iii) No differences were detected between active and non-active SLE or high- and low-dose corticosteroid patients. (iv) In SLE, increases in GR-DNA binding were associated with increases in NFκB-DNA binding (p < 0.0001), and increases in nuclear JNK were associated with increases in AP-1-DNA binding (p < 0.01). (v) In controls, increases in GR-DNA binding were associated with increases in AP-1-DNA binding (p < 0.001). Conclusion: We suggest disturbed GR, NFκB, AP-1 and JNK signaling in SLE, characterized by a reduced GR- and NFκB-DNA binding, a significant association between GR-mediated and NFκB-driven pathways, and a significant correlation between nuclear JNK- and AP-1-driven pathways. These disturbances may contribute to abnormal cytokine production and the etiopathogenesis of SLE. Copyright © 2006 S. Karger AG. |
en |
| heal.journalName |
NeuroImmunoModulation |
en |
| dc.identifier.issue |
4 |
en |
| dc.identifier.volume |
13 |
en |
| dc.identifier.doi |
10.1159/000100474 |
en |
| dc.identifier.spage |
194 |
en |
| dc.identifier.epage |
204 |
en |