Table 1.
MicroRNAs targeting Pim kinase in cardiovascular cell types.
MicroRNA | Target | Cell Type | Result | Ref |
---|---|---|---|---|
MiR-328 | Pim-1 | Pulmonary artery smooth muscle cells. Human umbilical vein endothelial cells |
Overexpression of MiR-328 increases the level of Pim-1 and promotes proliferation. Inhibition of MiRNA-328 promotes angiogenesis in high glucose conditions by increasing Pim-1 expression. |
[46,47] |
MiR-214 | Pim-1 | Bone marrow-derived mesenchymal stem cells Vascular smooth muscle cells |
PDGF increases the expression of this MiRNA, resulting in Pim-1 knockdown. | [32] |
MiR-206 | Pim-1 | Mesenchymal stem cells in hypoxia Pulmonary artery smooth muscle cells. |
Reduction in miR-206 causes increased proliferation and reduced apoptosis, which is protective in infarcted hearts. | [36,48] |
Mir-1 | Pim-1 | Vascular smooth muscle cells | Myocardin increases the expression of Mir-1, which results in the inhibition of VSMC proliferation via the knockdown of Pim-1. | [49] |
miR 410-5-p | Pim-1 | Diabetic cardiomyopathy | MiR-410-5p inhibition decreases high glucose-induced myocardial apoptosis, preventing cardiomyopathy through the upregulation of Pim-1. | [50] |
MiR-195 | Pim-1 | Sepsis—endothelial cells | Inhibition of miR-195 results in increased Pim-1, which is protective in a model of sepsis. | [51,52] |