Deficiency of lncRNA SNHG12 impairs ischemic limb neovascularization by altering an endothelial cell cycle pathway.

Gene set enrichment analysis (GSEA) using process networks from MetaCore Pathway Analysis showed that the common pathways dysregulated between SNHG12 and IMP3 were all highly significant ( Figure 8B ).

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Ischemia scores for these mice showed a significant trend toward increased ischemia ( Supplemental Figure 6E ).

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The antiangiogenic factor thrombospondin-2 (THBS2) is significantly increased in CLI patients relative to healthy adults and ischemic claudicants, and there is a nonsignificant trend toward increased expression in thrombospondin-1 (THBS1) ( 22 ).

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The percentage of non-myofiber area (extracellular matrix) was modestly increased in SNHG12-knockdown db/db mice; however, this did not reach statistical significance.

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Toe ischemia scores showed a trend toward more severe phenotype in comparison with C57BL/6 mice, consistent with what is generally observed in BALB/c mice undergoing FAL ( Supplemental Figure 5E ).

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