ABSTRACT
Ischemia-reperfusion (I-R) is renowned as a key approach in recovery related to cerebral infarction and further promotes succeeding infarction development. This study investigated the fundamental molecular function of the TALNEC2 in the pathogenesis of cerebral infarction to provide insights on the potential novel therapeutic agents in cerebral infarction. RT-qPCR measured expression of TALNEC2 and JNK in human neural cell line SH-SY5Y. Cell transfection upregulated or silenced the genes with MTT assay examining cell viability. RT-qPCR detected cell death in the apoptosis biomarker caspase-3, inflammation in the biomarkers C-reactive protein (CRP) and IL-6 and verified cell proliferation via the ki67 and PCNA markers. Luciferase assay was performed to see the luciferase activity and western blotting determined the protein expression of JNK in proliferation, inflammation. The results demonstrated that TALNEC2 was highly expressed after OGD/R treatment in nerve cells after cerebral infarction. In addition, TALNEC2 silencing prevented apoptosis and inflammation of nerve cells after cerebral infarction. TALNEC2 directly interacted with miR-19a-3p to regulate JNK protein expression. Lastly, miR-19a-3p inhibitor abolished the protective effect of si-TALNEC2 against OGD/R induced damage in vitro. In summary, this study has demonstrated that TALNEC2 is a positive moderator for pathogenesis of cerebral infarction. Furthermore, our conclusions provide further insights on the interplay among TALNEC2, miR-19a-3p and JNK in cerebral infarction. It has demonstrated herein that TALNEC2 positively modulates JNK post-transcriptional expression through miR-19a-3p sponging in cerebral Infarction offering a novel therapy target for cerebral infarction.
Subject(s)
Brain Ischemia , MicroRNAs , Neuroblastoma , RNA, Long Noncoding , Reperfusion Injury , Stroke , Animals , Apoptosis/genetics , Brain Ischemia/genetics , Brain Ischemia/metabolism , C-Reactive Protein , Caspase 3 , Cerebral Infarction/genetics , Glucose/pharmacology , Humans , Inflammation , Interleukin-6/pharmacology , Ki-67 Antigen , MicroRNAs/genetics , MicroRNAs/metabolism , Proliferating Cell Nuclear Antigen , RNA, Long Noncoding/genetics , Rats , Reperfusion Injury/metabolismABSTRACT
INTRODUCTION: Acute cerebral infarction (ACI) occurs with the involvement of differential expression of microRNAs. The study detected the expression pattern of miR-138-5p in the serum of ACI cases and evaluated its clinical significance, in an attempt to provide some guidance for the treatment and daily nursing of patients with ACI clinically. METHODS: Levels of miR-138-5p in the serum of ACI patients and healthy controls (HCs) were detected via qRT-PCR. Ninety days after treatment, the modified Rankin Scale (mRS) was used to evaluate the prognosis of ACI patients. Receiver operating characteristic (ROC) curve was drawn, and the area under the curve was calculated. The logistic regression analysis was performed to estimate the relationship between various indicators and the clinical outcome. RESULTS: miR-138-5p showed a diminished trend in ACI cases compared with the control group. A significantly negative correlation was detected for serum miR-138-5p with the National Institutes of Health Stroke Scale score in all ACI cases (r = -0.704, p < 0.001). The ROC curve demonstrated the diagnostic potential of serum miR-138-5p to distinguish ACI from HCs. Lessened expression of miR-138-5p was detected in ACI patients with poor prognosis, which can predict the poor prognosis of ACI patients after treatment. Logistic regression analysis determined the independent influence relationship between miR-138-5p and poor prognosis. CONCLUSION: Diminished miR-138-5p is identified to be a risk factor for the occurrence of ACI, and it is associated with the worse outcome of the patients.
