title: Elevated plasma CaM expression in patients with acute cerebral infarction predicts poor outcomes and is inversely associated with miR-26b expression.
abstract: BACKGROUND
  Calcium overload plays an important role in ischemia/reperfusion injury during ischemic brain damage and is mediated by calmodulin (CaM). However, the understanding of the regulatory mechanisms of CaM expression at the gene level is limited. The expression levels of miR-26b change significantly during ACI, and bioinformatic analyses predict that miR-26b would be a potential regulator of calmodulin (CALM1) mRNA. This study aimed to determine the expression of miR-26b and CaM in the plasma of patients with ACI and investigate the impact of miR-26b on CALM1 expression.
  
  
  METHODS
  CaM and miR-26b expression analyses from the plasma of patients with ACI and normal controls were performed using ELISA and qRT-PCR, respectively. Correlations between CaM, miR-26b, and NIHSS scores were analyzed. Then, miR-26b mimics and inhibitors were transfected into HUVE cell lines via lipofectamine. CALM1 mRNA expression in HUVECs was detected by RT-PCR, and the protein levels were detected by Western blot.
  
  
  RESULTS
  Plasma CaM expression in patients with ACI was significantly higher when compared with normal controls, and miR-26b expression was significantly lower. The plasma levels of CaM and miR-26b were correlated with the NIHSS scores in ACI patients. miR-26b modulated CALM1 in vitro. The transfected miR-26b mimic and inhibitor significantly altered the expression of CALM1/CAM at the mRNA and protein levels in cultured HUVECs.
  
  
  CONCLUSIONS
  CaM might be a potential novel blood marker in patients with ACI. miR-26b targeted CALM1 and affected the expression of CaM at the post-transcriptional level, which likely contributed to the progression of ACI brain injury.
authors.affiliation: b Department of Neurology, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Mei
authors.initials: M
authors.lastname: Yuan
authors.affiliation: b Department of Neurology, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Yonghong
authors.initials: Y
authors.lastname: Tang
authors.affiliation: b Department of Neurology, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Chengfang
authors.initials: C
authors.lastname: Zhou
authors.affiliation: b Department of Neurology, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Feng
authors.initials: F
authors.lastname: Liu
authors.affiliation: b Department of Neurology, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Lin
authors.initials: L
authors.lastname: Chen
authors.affiliation: a Department of Emergency, The second affiliated Hospital , University of South China , Hengyang , China.
authors.forename: Haijun
authors.initials: H
authors.lastname: Yuan
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002147:Calmodulin / Q000097:blood*; D002544:Cerebral Infarction / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000097:blood*; D008875:Middle Aged; D011379:Prognosis
chemical_list: D015415:Biomarkers; D002147:Calmodulin; D035683:MicroRNAs; C528163:MIRN26 microRNA, human
keywords: Acute cerebral infarction; NIHSS; calmodulin; miRNA-26b