Can MiR-503 be used as a marker in diabetic patients with ischemic stroke?

ABSTRACT

BACKGROUND: Some microRNAs are involved in diabetes pathology and some are known to have role in stroke. MiR-503 causes endothelial dysfunction in diabetic patients, predisposing to ischemia. There has been no study evaluating Mir-503 level in diabetic patients with or without ischemic stroke. METHODS: We designed a cross-sectional study to assess and compare serum level of MiR-503 in 4 groups of diabetic patients with ischemic stroke (I), non-diabetic patients with stroke (II), diabetic patients (III), and healthy controls (IV) in acute phase and 3 months later. RESULTS: Our data analysis showed that mean relative expression of MiR-503 in group (I) was significantly higher than 3 other groups (p < 0.05). The level of miR-503 was related to the patients' fasting blood glucose, Cholesterol level, NIHSS score and acute-phase modified Rankin Scale (mRS) (r = 0.49, p = 0.001, r = 0.5, p = 0.009, r = 0.45, p = 0.009, r = 0.48, p = 0.003, CI = 95%). Relative expression of miR in patients with mRS ≤ 2 (good outcome) was lower than in patients with mRS > 2 (poor outcome) (p = 0.008). After 3 months, level of miR decreased significantly only in group (I) (p = 0.002). Mean relative expression of miR-503 in chronic phase was not significantly different among groups (p-value> 0.05). There was no relation between miRNA level and mRS in chronic phase. CONCLUSION: Hyperglycemia and ischemia together raise the level of MiR-503 acutely but it does not remain at high level after 3 months. Although higher miR was related to more disability in acute phase, it does not affect long-term outcome in ischemic patients. As MiR-503 is stable enough in blood it can be used as a potential diagnostic marker of an ischemic stroke in diabetic patient. Its level also is an indicator of stroke severity and patients' short-term outcome. It is recommended to study whether antagomiR-503 is a new therapeutic agent reducing the severity of and disability due to stroke.