Purpose: MicroRNAs (miRs) are small noncoding RNAs which negatively regulate the expression of targeted mRNA transcripts. Some miRs are already known to modulate angiogenesis. The p75 neurotrophin receptor (p75NTR) is upregulated in endothelial cells (ECs) of diabetic models and contributes to impaired post-ischaemic reparative angiogenesis in diabetes. To elucidate the miR signature of p75NTR in ECs, human umbilical vein ECs (HUVECs) infected with Ad.p75NTR demonstrated the upregulation of miR-30c-2* on an array. We aim to characterize the impact of miR-30c-2* on EC function. Methods: Array results were confirmed by q-PCR using validated miR primers and SnU6 as an internal reference. To mimic advanced diabetes, where hyperglycaemia is accompanied by tissue starvation, HUVECs were cultured in high D-glucose (HG, 25 mM) and low growth factors (LGF). For modulating miR expression, HUVECs were transfected with pre-miR precursor, anti-miR inhibitor or negative control. Transfected cells were prompted in proliferation (BrdU incorporation) and in vitro angiogenesis on Matrigel assays. Predicted miR target genes were searched using the databases Microcosm and TargetScan. Finally, relative miR-expression was quantified in limb muscles of type 2 diabetic db/db mice and non-diabetic controls. Statistical analyses are performed using either an unpaired t-test (two groups) or ANOVA (more than two groups). Results: Relative expression of miR-30c-2* was upregulated (three-fold) in p75NTR-transduced HUVECs (p<0.01 vs. null-HUVECs) and five-fold in HG/LGF compared to culture in normal conditions (p<0.01). Overexpression of miR-30c-2* in HUVECs impaired both proliferation and angiogenesis (40% decrease in proliferation and 25% decrease in tube length of Matrigel network, p<0.01 for both). In addition, miR-30c-2* was upregulated three-fold in the adductor muscles of db/db diabetic mice (p<0.05 vs. non-diabetic controls). A bioinformatics analysis identified the cell cycle regulator minichromosome maintenance complex component 7 (MCM7) as a putative miR-30c-2* target, In line, MCM-7 mRNA levels were decreased in p75NTR-HUVECs (by 57% vs. Null-HUVECs, p<0.05) and in HUVECs cultured in HG/LGF. Overexpression of miR-30c-2* also reduced MCM7 mRNA (by 64%, p<0.01). Conclusion: Our data suggest that the p75NTR-induced miRNA miR-30c-2* may act as an anti-angiogenic mediator in the context of diabetes by inhibiting the cell cycle regulator MCM7. miR-30c-2* may prove to be a novel therapeutic target for diabetes-induced impairment of post-ischaemic reparative neovascularisation.