Cell lines

Brain endothelial cells

Preparation method

The solubility of this compound in sterile water is 0.50 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months.

Reacting condition

0 ~ 50 μg/mL; 48 hrs

Applications

MOG (35-55) significantly decreased the protein concentration in a dose-dependent manner. In cells treated with MOG (35-55) (50 μg/mL) + CFA + PTX, the protein concentration decreased to 37.6% of the level in the CON cells. At the doses of 25 or 50 μg/mL, MOG (35-55) emulsion substantially increased the activities of NADPH oxidase and MMP-9 (44.1 ~ 48.5% and 2-fold higher than those in the CON cells, respectively).

Animal models

C57BL/6 mice

Dosage form

50, 100 or 150 μg; s.c.

Applications

At the doses of 50 and 100 μg, MOG (35-55) induced more dramatic weight losses during the course of the MS-like disease, when compared with mice injected with 150 μg MOG (35-55). At day 17 after treatment, 3/5 mice in the 50 μg MOG (35-55) group were moribund whereas 4/5 mice still survived in the 100 and 150 μg dose groups. However, no clinical sign and disease progression were observed in these 3 groups of mice.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

MOG (35-55) is a truncated peptide derived from the human Myelin Oligodendrocyte Glycoprotein (MOG). MOG, a member of the immunoglobulin superfamily, is expressed wildly in the central nervous system. In mouse and rat models for human multiple sclerosis, MOG is involved in inducing the experimental autoimmune encephalomyelitis. Humoral auto-immunity to the myelin oligodendrocyte glycoprotein (MOG) may be associated with the pathogenesis of multiple sclerosis (MS) [1].

MOG (35-55) is involved in inducing autoantibody production and relapsing-remitting neurological disease causing extensive plaque-like demyelination [2]. In HLA-DR2-transgenic mice, Myelin oligodendrocyte glycoprotein-35-55 peptide induced severe chronic experimental autoimmune encephalomyelitis [3].MOG35-55 was highly encephalitogenic and could induce strong T and B cell responses in rats [4]. In NOD/Lt mice (H-2g7) and C57BL/6 mice (H-2b), single injection of MOG35-55 in CFA could induce MS-like disease [4].

References:
[1]. De March A K, De Bouwerie M, Kolopp-Sarda M N, et al. Anti-myelin oligodendrocyte glycoprotein B-cell responses in multiple sclerosis[J]. Journal of neuroimmunology, 2003, 135(1): 117-125.
[2]. Slavin A, Ewing C, Liu J, et al. Induction of a multiple sclerosis-like disease in mice with an immunodominant epitope of myelin oligodendrocyte glycoprotein[J]. Autoimmunity, 1998, 28(2): 109-120.
[3]. Rich C, Link J M, Zamora A, et al. Myelin oligodendrocyte glycoprotein‐35–55 peptide induces severe chronic experimental autoimmune encephalomyelitis in HLA‐DR2‐ ransgenic mice[J]. European journal of immunology, 2004, 34(5): 1251-1261.
[4]. Slavin A, Ewing C, Liu J, et al. Induction of a multiple sclerosis-like disease in mice with an immunodominant epitope of myelin oligodendrocyte glycoprotein[J]. Autoimmunity, 1998, 28(2): 109-120.