Study on the Effect and Mechanism of miR-185 on Lower Extremity Deep Venous Thrombosis

Mol Biotechnol. 2022 Mar;64(3):330-337. doi: 10.1007/s12033-021-00412-w. Epub 2021 Oct 14.

Abstract

Lower extremity deep venous thrombosis (LEDVT) is a venous reflux disorder caused by abnormal coagulation of blood. LEDVT can obstruct the lumen and LEDVT is the third vascular disease after cerebrovascular diseases and coronary artery diseases. miRNAs are associated with thrombosis, and miR-185 was reported to affect the proliferation and apoptosis of vascular endothelial cells by regulating receptor of advanced glycation end products (RAGE). However, no study has reported the effect of miR-185 on LEDVT. Here, we studied the effects of miR-185 on the PI3K/AKT and MAPK signaling pathways in the LEDVT cells. The results showed that miR-185 promotes cell proliferation through activating the PI3K/AKT and MAPK signaling pathways and then inhibits tissue factor and fibrin expression to reduce thrombosis. In short, our study provides new ideas and a theoretical basis for research on the prevention, diagnosis, and treatment of LEDVT.

Keywords: AKT; Fibrin; Lower extremity deep venous thrombosis; PI3K/AKT; Tissue factor; miR-185.

MeSH terms

  • Animals
  • Cell Proliferation
  • Cells, Cultured
  • Chromones / pharmacology
  • Disease Models, Animal
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Fibrin / metabolism
  • MAP Kinase Signaling System
  • Male
  • Mice
  • MicroRNAs / genetics*
  • Morpholines / pharmacology
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Rats
  • Thromboplastin / metabolism
  • Venous Thrombosis / etiology
  • Venous Thrombosis / genetics*
  • Venous Thrombosis / metabolism

Substances

  • Chromones
  • MIRN185 microRNA, rat
  • MicroRNAs
  • Mirn185 microRNA, mouse
  • Morpholines
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Fibrin
  • Thromboplastin
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt