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Fig. 6 | Journal of Biomedical Science

Fig. 6

From: Hypoxic stress disrupts HGF/Met signaling in human trophoblasts: implications for the pathogenesis of preeclampsia

Fig. 6

Expression of Cbl and CAV-1 in the placentas of patients with E-PE and PTL. A, B Results of real-time quantitative PCR showing the relative expression of Cbl and CAV-1 in the PTL (n = 7) and E-PE (n = 16) placentas. C Typical results of Western blotting showing the protein levels of Cbl and CAV-1 in the PTL (n = 7) and E-PE (n = 16) placentas. D, E Bar chart showing the relative densities of Cbl and CAV-1. F Working model illustrating the endocytosis and degradation of Met in trophoblasts under physiological normoxic and pathologically sustained hypoxic conditions. Under normoxic conditions (left panel), the binding of HGF to Met activates Met-Erk signaling to enhance trophoblast invasion and induce CAV-1-coupled endocytosis and the subsequent Cbl-mediated degradation of Met, thereby maintaining the homeostasis of HGF/Met signaling in placental trophoblasts. However, when trophoblasts face prolonged hypoxic stress (right panel), the augmented endocytosis via CAV-1 and hampered Cbl-mediated degradation of Met lead to the aberrant intracellular accumulation of Met and thus to the impaired activation of Met/Erk signaling and dysregulation of trophoblast differentiation. The data are expressed as the mean ± SEM and were analyzed by the two-tailed t test based on at least three independent experiments. *Compared with the corresponding data in the control, p < 0.05

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