Increased Plasma Matrix Metalloproteinase-9 Levels in Migraineurs

Department of Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.
Headache The Journal of Head and Face Pain (Impact Factor: 2.71). 01/2008; 48(1):135-9. DOI: 10.1111/j.1526-4610.2007.00958.x
Source: PubMed


Cortical spreading depression and neurogenic inflammation have been hypothesized to be key steps in the development of migraine headache. Recent studies have highlighted matrix metalloproteinase-9 (MMP-9) in cortical spreading depression, neurogenic inflammation, and cerebral ischemia. To seek their possible association, we investigated plasma MMP-9 levels in migraineurs during headache-free periods.
Plasma MMP-9 levels in 84 migraine subjects and 61 controls were determined by enzyme-linked immunosorbent assay. In addition, 23 patients with tension type headache were included in the study as comparative subjects.
The MMP-9 levels in migraineurs (42.5+/-4.6 ng/mL, mean+/-SE) were significantly higher than those in controls (25.4+/-2.7 ng/mL, P< .005). Those levels in tension type headache subjects (24.6+/-4.8 ng/mL) did not differ from those in controls. There was no significant difference between subjects having migraine with aura and those without aura. The MMP-9 levels did not correlate with age, duration of illness, frequency of migraine attack, duration of headache attack, or medication for headache. Mean plasma MMP-9 levels were the highest in subjects from whom blood samples were taken 2-4 days after their latest attack.
The degradation of extracellular matrix showing the increase of MMP-9 in migraineurs may be associated with an abnormality in their blood vessel permeability. MPP-9 plays some role in migraine pathophysiology. Further studies of MMPs are necessary to elucidate their role.

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    • "Of the 80 DEGs, we selected the following 12 genes on the basis of a thorough literature review: HLA class II beta chain 1 (HLA-DRB1), HLA-A29.1, HLA class II beta chain 6 (HLA-DRB6) [13], MMP9 [14], prostaglandin-endoperoxide synthase 2 (PTGS2) [15], IL-8 [16], MMP25 [17], alanine aminopeptidase N (ANPEP, or CD13) [18], l-histidine decarboxylase (HDC) [19], G-CSF3R [20], STAT3 [21], and Rho guanine nucleotide exchange factor 10 (ARHGEF10) [22]. Compared to controls, HLA-DRB1, HLA-A29.1, "
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