Figure 7.

miR-143-3p protects against apoptosis in endothelial and vascular smooth muscle cells by targeting IGF-IIR. (A) Relative quantification of the expression levels of miR-143-3p in transfected HUVECs (left) and VSMCs (right). (B) Representative Western blot images of IGF-IIR expression (upper) and their quantification (lower) in transfected HUVECs (left panels) and VSMCs (right panels). (C) Representative Western blot images of IGF-IIR expression (upper) and their quantification (lower) in murine aorta samples. (D) Representative immunohistochemical analysis of IGF-IIR expression in advanced carotid atherosclerosis patients (upper) and its quantification (lower) expressed in %positive staining/mm² in the different areas of the atherosclerotic plaque. Magnification 40× (scale bar = 200 µm). (E) Representative Western blot images of active caspase 3 (upper) and their quantification (lower) in transfected HUVECs following serum deprivation (left) and transfected VSMCs following thapsigargin exposure (right). HUVECs = human umbilical vein endothelial cells; VSMCs = vascular smooth muscle cells; IGF-IIR= insulin-like growth factor type 2 receptor; WT = Wild type group; STD = standard type diet; ApoE^−/− = ApoE deficient mice; HFD = high fat diet; IHC = immunohistochemistry; M = media; F = fibrous; S = shoulder; FBS = foetal bovine serum. All the in vitro experiments have been performed at least 3 times (n = 3). Western blot of IGF-IIR: WT STD 18 wks (n = 6); ApoE^−/− STD 18 wks (n = 6); ApoE^−/− HFD 18 wks (n = 6). Immunohistochemistry of IGF-IIR: Media (n = 44); Fibrous (n = 49); Shoulder (n = 19).