| Autor: |
asadikaram, Gholamreza, Noroozi, Saam, Ebrahimi Meimand, Hossein ali, Sanjari, Mojgan, Zainodini, Nahid, Khoramdelazad, Hossein, Shahrokhi, Nader, Kazemi arababadi, Mohammad |
| Zdroj: |
Neuroimmunomodulation; May2017, Vol. 23 Issue 5/6, p345-351, 7p |
| Abstrakt: |
Objectives: Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules. Methods: S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy. Results: S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB. Conclusions: It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-inde-pendent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
