Circulatory microRNA-145 expression is increased in cerebral ischemia.

نویسندگان

  • C S Gan
  • C W Wang
  • K S Tan
چکیده

Cerebral ischemia or ischemic stroke is mainly attributed to vascular and circulation disorders. Among protein biomarkers, RNA profiles have also been identified as markers of ischemic stroke. MicroRNA-145 expression is ostensibly recognized as marker and modulator of vascular smooth muscle cell phenotype; however, expression levels in ischemic stroke had not been investigated. Employing real-time quantitative PCR, we examined the expression profile of circulatory microRNA-145 in healthy control subjects (N = 14) and ischemic stroke patients (N = 32). Circulatory microRNA-145 expression was significantly higher in ischemic stroke patients than in control subjects. This demonstrates that hemostatic mechanisms are affected by ischemic stroke. We conclude that circulating microRNA-145 has potential as a biomarker for ischemic stroke.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effects of Usnic Acid on Apoptosis and Expression of Bax and Bcl-2 Proteins in Hippocampal CA1 Neurons Following Cerebral Ischemia-Reperfusion

Introduction: Cerebral ischemia-reperfusion causes complex pathological mechanisms that lead to tissue damage, such as neuronal apoptosis. Usnic acid is a secondary metabolite of lichen and has various biological properties including antioxidant and anti-inflammatory activities. This study aimed to investigate the neuroprotective effects of usnic acid on apoptotic cell death and apoptotic-relat...

متن کامل

Overexpression of MicroRNA-145 Ameliorates Astrocyte Injury by Targeting Aquaporin 4 in Cerebral Ischemic Stroke

Cerebral ischemic stroke, which affects the global population, is a major disease with high incidence, mortality, and disability. Accumulating evidence has indicated that abnormal microRNA (miRNA) expression plays essential roles in the pathologies of ischemic stroke. Yet, the underlying regulatory mechanism of miRNAs in cerebral ischemic stroke remains unclear. We investigated the role of miR-...

متن کامل

Protective Effects of Nucleobinding-2 After Cerebral Ischemia Via ‎Modulating Bcl-2/Bax Ratio and Reducing Glial Fibrillary Acid Protein ‎Expression

Introduction: Nucleobinding-2 (NUCB2) or nesfatin-1, a newly identified anorexigenic peptide, has antioxidant, anti-inflammatory, and anti-apoptotic properties. Brain ischemia-reperfusion induces irreversible damages, especially in the hippocampus area. However, the therapeutic effects of NUCB2 have not been well investigated in cerebral ischemia. This study was designed for the first time to i...

متن کامل

Expression profiles of microRNAs after focal cerebral ischemia/reperfusion injury in rats☆

Rat models of focal cerebral ischemia/reperfusion injury were established by occlusion of the middle cerebral artery. Microarray analysis showed that 24 hours after cerebral ischemia, there were nine up-regulated and 27 down-regulated microRNA genes in cortical tissue. Bioinformatic analysis showed that bcl-2 was the target gene of microRNA-384-5p and microRNA-494, and caspase-3 was the target ...

متن کامل

Bad gene expression following effect of coenzyme Q10 on Wistar rat hippocampus with cerebral ischemia

Background: Q10 coenzyme is a potent antioxidant in the mitochondrial membrane. Releasing the oxygen free radicals occurs in the cerebral ischemia. Using Q10 coenzyme causes strength against oxidative after injury of cerebral ischemia during reperfusion. Also CoQ10 plays an important anti-apoptotic role to reduce Caspase 3 as a key enzyme neuroprotective in apoptosis. According to the sensitive...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Genetics and molecular research : GMR

دوره 11 1  شماره 

صفحات  -

تاریخ انتشار 2012