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. Author manuscript; available in PMC: 2015 Mar 18.
Published in final edited form as: FEBS Lett. 2014 Jan 31;588(6):906–914. doi: 10.1016/j.febslet.2014.01.033

Figure 5. Proposed Model of cytokine induced, miR-138-mediated, EC dysfunction.

Figure 5

(1) Engagement of vasocative or pro-inflammatory cytokine receptors by their respective ligands leads to stabilization of HIF1-α in ECs through as yet incompletely defined mechanisms (2). Stabilization of HIF1-α increases miR-138 levels (3), which destabilize S100A1 mRNA or suppress its translation, leading to rapid loss of S100A1 protein in ECs (4). This leads to increased phospho-Thr495 eNOS levels (5) with consequent reduction of NO generation (6). This loss of endothelial NO generation engenders endothelial dysfunction (7).