<p>Parkinson’s disease (PD) is a widespread neurodegenerative disorder. MicroRNAs (miRNAs) have emerged as crucial regulatory molecules in the context of PD. Exploring the diagnostic significance of miR-4443 in PD and its impacts on microglial inflammatory responses. The present study enrolled 95 PD patients and 90 healthy controls. The expression levels of miR-4443 and EBF3 and their diagnostic potential for PD were analyzed using RT-qPCR and a ROC curve. LPS-treated BV2 microglial cells were utilized to simulate the neuroinflammatory process in PD pathogenesis. Cell proliferation activity was assessed using the CCK-8 assay. ELISA was employed to measure cellular pro-inflammatory cytokine levels. To confirm the putative binding between miR-4443 and EBF3, a dual-luciferase reporter assay was conducted. The expression level of miR-4443 was significantly up-regulated in the serum of PD patients, and it exhibited diagnostic potential for PD. Following LPS induction in BV2 microglial cells, miR-4443 expression was up-regulated. Overexpression of this miRNA suppressed proliferation and enhanced pro-inflammatory cytokine release. Conversely, miR-4443 knockdown reversed the resultant phenotypic changes. EBF3 was verified to have a binding relationship with miR-4443. Functional experiments indicated that miR-4443 might participate in the neuroinflammatory process of PD pathogenesis by targeting EBF3. Up-regulated miR-4443 has diagnostic significance for PD and may participate in neuroinflammation through regulating EBF3.</p> Graphical Abstract <p></p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Up-regulated miR-4443 Holds Diagnostic Significance for Parkinson’s Disease and may be Involved in Neuroinflammation

  • Huijie Lu,
  • Zhenwu Zhao,
  • Yang Lin,
  • Siying Lei,
  • Yuyao Feng

摘要

Parkinson’s disease (PD) is a widespread neurodegenerative disorder. MicroRNAs (miRNAs) have emerged as crucial regulatory molecules in the context of PD. Exploring the diagnostic significance of miR-4443 in PD and its impacts on microglial inflammatory responses. The present study enrolled 95 PD patients and 90 healthy controls. The expression levels of miR-4443 and EBF3 and their diagnostic potential for PD were analyzed using RT-qPCR and a ROC curve. LPS-treated BV2 microglial cells were utilized to simulate the neuroinflammatory process in PD pathogenesis. Cell proliferation activity was assessed using the CCK-8 assay. ELISA was employed to measure cellular pro-inflammatory cytokine levels. To confirm the putative binding between miR-4443 and EBF3, a dual-luciferase reporter assay was conducted. The expression level of miR-4443 was significantly up-regulated in the serum of PD patients, and it exhibited diagnostic potential for PD. Following LPS induction in BV2 microglial cells, miR-4443 expression was up-regulated. Overexpression of this miRNA suppressed proliferation and enhanced pro-inflammatory cytokine release. Conversely, miR-4443 knockdown reversed the resultant phenotypic changes. EBF3 was verified to have a binding relationship with miR-4443. Functional experiments indicated that miR-4443 might participate in the neuroinflammatory process of PD pathogenesis by targeting EBF3. Up-regulated miR-4443 has diagnostic significance for PD and may participate in neuroinflammation through regulating EBF3.

Graphical Abstract