Figure 2.

miR-200c and miR-33 interplay in psoriasis and CVD. miR-200c and miR-33 positively correlate in plasma and plaques of atherosclerotic patients. A molecular mechanism among miR-33a/b and miR-200c increase does exist. Indeed, the overexpression of miR-33a/b in vitro in different cells (i.e. ECs, hepatic cells and embryonic kidney cells) causes the intracellular and extracellular increase of miR-200c via a ZEB1-decrease mechanism. ZEB1, in fact, is a direct target of both miR-33 and miR-200c and a transcriptional inhibitor of miR-200c. Hence, a ZEB1-decrease causes upregulation of both intracellular and extracellular miR-200c expression levels. An increase of miR-200c in skin plaques and plasma of psoriatic patients was also observed, and it positively correlates with PASI index and determinants of CVD risk (RWT, E/e’ and LV mass). Interestingly, miR-33a was found to be upregulated in the plasma of psoriatic patients and positively correlates with HOMA-insulin resistance index and cIMT. Therefore, a possible link in psoriasis could also exist among miR-33 and miR-200c, contributing to the increase of CVD in these patients.