Background and Objective: Transcription factors (TF) and microRNAs, are the largest families of transacting gene regulatory molecules in multicellular organisms. Our goal was to examine the effect of aerobic running on the expression of miR-124 and RE1-silencing TF in the hippocampus of adult male Wistar rats.Materials and Methods: A total of twelve 8-week-old adult male Wistar rats with a mean body weight of 200-225 g were selected as subjects. Following 1 week of familiarization, the animals were randomly divided into two groups of test (n=6) and control (n=6). In the test group, animals were forced to run on a treadmill, at a speed of 25 m/min for 30 minutes per day, for 14 consecutive days. The animals were sacrificed 24 hours after the last exercise session, and the hippocampi were removed from both sides of the brain hemispheres. Changes in the expression of miR-124 and RE1-silencing TF were analyzed using the quantitative RT-PCR technique.Results: Statistical analysis by independent sample t-test, showed that there was a significant difference between the exercise and control groups (P£0.05), and while exercise significantly elevated the expression of miR-124, it reduced the expression of RE1-silencing TF.Conclusion: Our findings show that forced aerobic running at a speed of 25 m/min could lead to positive changes in mechanisms involved in exercise-induced neurogenesis.

Dear Editor, Metabolic syndrome (MS) represents a cluster of cardiovascular risk factors (obesity, hypertension, dyslipidemia and insulin resistance) associated with increased cardiovascular morbidity and mortality. The genetic basis of MS is still unknown and very important to be determined because of constantly increasing prevalence of MS worldwide, which is primarily due to epidemic obesity. Mitochondrial transcription factor A (TFAM) plays an essential role in direct regulation of mitochondrial genome, affecting transcription initiation and replication. Age-related modifications of oxidative stress could impact mitochondrial DNA replication by regulating the TFAM activity in type II diabetes.