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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2011 Jan 6;31(4):890–897. doi: 10.1161/ATVBAHA.110.215640

Figure 2. DDAH1 siRNA in HUVEC attenuated tube formation, proliferation, p-AktSer473 and p-eNOSSer1177.

Figure 2

Figure 2

DDAH1 siRNA attenuated HUVEC tube formation on Matrigel (A,B) and cell proliferation (C). 24 hours post transfection with siRNA, HUVEC cell number was counted and layered on Matrigel; tube structures were observed 18 hours later. Tube length was decreased in cells transfected with DDAH1 siRNA compared to control siRNA (n=4/group). D: ADMA (5-100 μM) inhibits HUVEC proliferation in a concentration dependent manner. E: The nonselective NOS inhibitor L-NAME (5mM) and the soluble guanylyl cyclase inhibitor ODQ (1μM) attenuated HUVEC proliferation. F: The permeable cGMP analogue PCMPT (1-50μM) dose dependently rescued the decrease of HUVEC proliferation caused by DDAH1 siRNA. G and H: DDAH1 siRNA decreased DDAH1, p-AktSer473 and p-eNOSSer1177 but had no effect on total-Akt or total-eNOS. I: The decrease of HUVEC proliferation caused by DDAH1 siRNA was totally rescued by overexpression of constitutively active Akt (MOI 50)(C). *p<0.05 as compared with control conditions.