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. 2018 May 14;9(5):576. doi: 10.1038/s41419-018-0567-0

Fig. 5. The degradation of Cav-1 is initiated by starvation-induced autophagy to promote LSECs defenestration.

Fig. 5

Primary rats LSECs, isolated from normal rats, were cultured without fetal bovine serum from 12 h till 48 h in vitro. a Protein levels of VEGFR2, p-PI3K (Tyr458), PI3K, p-AKT (Ser473), AKT, p-MTOR (Ser2448), and MTOR analyzed by western blot. The relative protein expression is quantified in the graph, down. *P < 0.05 versus VEGFR2/β-actin of the concurrent control group; #P < 0.05 versus p-PI3K/PI3K of the concurrent control group; &P < 0.05 versus p-AKT/AKT of the concurrent control group; $P < 0.05 versus p-MTOR/MTOR of the concurrent control group. b Red or yellow represents autolysosomes or autophagosomes, respectively, visualized by confocal microscopy. Quantification of autophagic flux (%) in 100 cells was analyzed. *P < 0.05 versus the autolysosomes of the concurrent control group; #P < 0.05 versus the autophagosomes of the concurrent control group. c Protein levels of LC3 II/I, Cav-1, p-eNOS (Ser1177), eNOS, p-VASP (Ser157), and VASP in primary LSECs analyzed by western blot. The relative protein expression is quantified in the graph, down. *P < 0.05 versus LC3 II/I of the concurrent control group; #P < 0.05 versus Cav-1/β-actin of the concurrent control group; &P < 0.05 versus p-eNOS/eNOS of the concurrent control group; $P < 0.05 versus p-VASP/VASP of the concurrent control group. d Magnification of SEM of LSECs in the CTR group and the Starvation group for 2 days, revealing the fenestrae structures (scale bar: 5 μm), and quantification of the total fenestral diameter, right. The black triangles indicate LSECs fenestrae structures. *P < 0.05 versus the concurrent control group