The role of fibrillin-1 protein and its associated miR-144-3p in the pathophysiology of stroke due to acute cervical artery dissection in humans

Objective: The aim of this study is to investigate the role of fibrillin-1 protein and its associated miR-144-3p in the pathophysiology of stroke due to acute cervical artery dissection (CAD). Cervical artery dissection is a significant cause of ischemic strokes in young adults, and its pathophysiology remains incompletely understood. Fibrillin-1 is a key component of the extracellular matrix and plays a critical role in maintaining connective tissue integrity. Additionally, miR-144-3p is known to influence vascular biology and inflammatory processes. In this context, examining the potential roles of fibrillin-1 and miR-144-3p in CAD-related stroke may contribute to a better understanding of the molecular mechanisms underlying this condition.. Method: The study compared 28 patients with CAD-related stroke, 28 patients with non- CAD stroke, and 28 healthy controls. Peripheral blood samples collected within the first 24 hours after stroke were analyzed for fibrillin-1 levels using the ELISA method and miR-144-3p expression using RT-PCR. These methods ensured precise and reliable measurement of the biomarkers. Results: The mean age of the SAD group was found to be significantly lower compared to the non-dissection ischemic stroke group (p = 0.01). No significant differences were observed between the groups in terms of risk factors. Although no overall significant difference was found in Fibrillin-1 concentration among the groups, a statistically significant difference was detected between the dissection and stroke groups (p = 0.042). No significant differences were observed between the groups in terms of DeltaCt, DeltaDeltaCt, and RelativeExpression values. Conclusion: The findings revealed no statistically significant differences in fibrillin-1 and miR-144-3p levels between the groups. These results suggest that fibrillin-1 and miR-144- 3p may not play a significant role in the pathophysiology of CAD-related stroke. However, further studies with larger sample sizes and different time points are needed to better understand the potential roles of these biomarkers.