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Fig. 8 | Reproductive Biology and Endocrinology

Fig. 8

From: Analysis of 17β-estradiol (E2) role in the regulation of corpus luteum function in pregnant rats: Involvement of IGFBP5 in the E2-mediated actions

Fig. 8

Effects of luteal E2 inhibition, replacement and androgen receptor antagonist on serum T, CL weight, IGFBP5 mRNA and protein levels. a and b circulating mean±SEM serum T concentrations and weight of CL during different treatments (n = 4 animals/time point and n = 12 CL/time point for weight calculation one-way ANOVA, *** P <0.001). c qPCR expression analysis of Igfbp5 in CL post different treatments. The results are shown as fold changes of mRNA expression compared with day 16 VEH group. Individual bars represents mean±SEM fold change during different treatments (n = 4 animals/time point, one-way ANOVA, *** P <0.001). d Immunoblot analysis of IGFBP5. A representative immunoblot is shown. β-actin was used as loading control for each lane. Each bar represents the fold change with respect to day 16 VEH and indicated as mean±SEM (n = 4 animals/time point), relative to intensity of β-actin for each treatment (one-way ANOVA, *** P <0.001). e Schematic representation of IGFBP5 modulation of classical IGF and E2 activated signalling pathways in the rat luteal cell. Increased IGFBP5 levels as a result of E2 inhibition by AI causes decrease in circulating IGF1 levels leading to decreased activation of IGF1R (a tyrosine kinase) resulting in decreased activation of PI3K and pAkt/PKB levels. Simultaneously, due to unavailability of E2 leads to inhibition of PI3K/Akt signalling pathway and thus inhibiting the survival pathway. E 2 17β-estradiol, ER estrogen receptor, IGFBP5 insulin- like growth factor binding protein 5, IGF1 insulin like growth factor 1, IGF1R IGF1 receptor, Src non receptor protein tyrosine kinase, SHC Src homology 2 domain containing transforming protein, GRB2 growth factor receptor bound protein 2, SOS Son of sevenless, PI3K, phosphatidylinositol 3-kinase, Akt protein kinase B, p phosphate group, ERE estrogen response element, AI aromatase inhibitor, ns non-significant

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