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10.1111/jcmm.15124

http://scihub22266oqcxt.onion/10.1111/jcmm.15124
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32147957!7176881!32147957
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suck abstract from ncbi


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pmid32147957      J+Cell+Mol+Med 2020 ; 24 (8): 4624-4632
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  • MiR-9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway #MMPMID32147957
  • Zhou DM; Sun LL; Zhu J; Chen B; Li XQ; Li WD
  • J Cell Mol Med 2020[Apr]; 24 (8): 4624-4632 PMID32147957show ga
  • Endothelial progenitor cells (EPCs) have emerged as a promising therapeutic choice for thrombi recanalization. However, this role of EPCs is confined by some detrimental factors. The aim of this study was to explore the role of the miR-9-5p in regulation of the proliferation, migration and angiogenesis of EPCs and the subsequent therapeutic role in thrombosis event. Wound healing, transwell assay, tube formation assay and in vivo angiogenesis assay were carried out to measure cell migration, invasion and angiogenic abilities, respectively. Western blot was performed to elucidate the relationship between miR-9-5p and TRPM7 in the autophagy pathway. It was found that miR-9-5p could promote migration, invasion and angiogenesis of EPCs by attenuating TRPM7 expression via activating PI3K/Akt/autophagy pathway. In conclusion, miR-9-5p, targets TRPM7 via the PI3K/Ak/autophagy pathway, thereby mediating cell proliferation, migration and angiogenesis in EPCs. Acting as a potential therapeutic target, miR-9-5p may play an important role in the prognosis of DVT.
  • |Animals[MESH]
  • |Autophagy/genetics[MESH]
  • |Cell Movement/genetics[MESH]
  • |Cell Proliferation/genetics[MESH]
  • |Endothelial Progenitor Cells/*metabolism/pathology[MESH]
  • |Gene Expression Regulation/genetics[MESH]
  • |Humans[MESH]
  • |Mice[MESH]
  • |MicroRNAs/*genetics[MESH]
  • |Morphogenesis/genetics[MESH]
  • |Neoplasm Invasiveness/genetics[MESH]
  • |Neovascularization, Pathologic/*genetics[MESH]
  • |Phosphatidylinositol 3-Kinases/genetics[MESH]
  • |Protein Serine-Threonine Kinases/*genetics[MESH]
  • |Proto-Oncogene Proteins c-akt/genetics[MESH]
  • |TRPM Cation Channels/*genetics[MESH]
  • |Thrombosis/*genetics/pathology/therapy[MESH]


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