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. Author manuscript; available in PMC: 2013 Apr 25.
Published in final edited form as: Circ Res. 2009 Sep 17;105(9):897–905. doi: 10.1161/CIRCRESAHA.109.199059

Figure 7. IGFBP-3 activates nitric oxide synthase and causes NO release by activating SR-B1/PI3-kinase/Akt pathway.

Figure 7

(A) NO production in response to IGFBP-3 was measured by DAF- FM fluorescence in HUVECs and effects of different pharmacological blockers were evaluated (color scale for fluorescence). Images obtained were cells that were either not treated (time control) or treated as labeled. (B) Changes in fluorescence with different treatments were expressed as percent increase over the time control. NO release by IGFBP-3 was significantly decreased by pretreatment with SR-B1 blocking antibody (SRB1-Ab), LY294002, triciribin or L- NAME. *P<0.01 and ***P<0.0001 compared with IGFBP-3. (C) eNOS activity expressed as L- NAME inhibitable conversion of [14C]L-arginine to [14C]L-citrulline was stimulated by 100 ng/ml IGFBP-3. Pretreatment with SRB1-Ab, 30 μM LY294002 or 30 μM triciribin significantly decreased IGFBP-3 induced eNOS activation (*P<0.05). Representative results from three independent experiments are shown.