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Breast Cancer Research and Treatment
Published online 2010 August 17. doi: 10.1007/s10549-010-1085-7

Fig. 2

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N-TSP2-Fc induces apoptosis of HDMEC by CD36 receptor-mediated loss of mitochondrial membrane potential and activation of caspase-3. Percentage of apoptotic HDMEC (a) was measured by flow cytometry. Treatment with N-TSP2-Fc resulted in a significant increase of HDMEC apoptosis (a). Concurrent addition of a blocking CD36 antibody (CD36 ab) with N-TSP2-Fc inhibited this effect (a). The percentage of mitochondrial membrane potential (b) was decreased after treatment of HDMEC with N-TSP2-Fc. Simultaneous incubation of N-TSP2-Fc with anti-CD36 antibody (CD36 ab) did not induce loss of mitochondrial membrane potential when compared to control HDMEC (b). Active caspase-3 was analyzed in HDMEC by western blot analysis (c). Image analysis (d) of the bands revealed that caspase-3 activity was increased by incubation of HDMEC with N-TSP2-Fc. Caspase-3 activity of control-treated HDMEC or HDMEC incubated with N-TSP2-Fc and concurrent addition of anti-CD36 antibody (CD36 ab) was comparable (d). In all experiments ad, HDMEC were incubated with PBS (control), or with 40 μg/ml of N-TSP2-Fc, or with 40 μg/ml of N-TSP2-Fc plus 10 μg/ml of blocking CD36 antibody. All experiments were performed in the presence of VEGF (20 ng/ml). Results are expressed as mean + SEM (n = 3). ** P < 0.01, *** P < 0.001

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