Fig. 7

Fig. 7

Irs2b mediates H₂O₂-dependent Erk1/2-phosphorylation and catch-up growth. (A) Immunoblot analysis of the IGF1 (200 ng/mL) -induced phosphorylation levels of Erk1/2 in the presence or absence of H₂O₂ and Irs2b in HEK293T cells. Cells harboring the irs2b overexpression (irs2b OE) or not (control) were used. Data are mean ± SE of 2 independent experiments. Values marked with different letters (a, b) are significantly different from each other (N.S. means not significantly different (P<0.05). (B) Changes in the relative growth rate of embryos in the Reoxy (32-45 hpf) embryos treated with or without VAS2870 and H₂O₂. Embryos lacking the irs2b expression (irs2b KD) or control MO injected embryos (Control) were used for experiments. The vehicle alone group was set as 100%. Data are mean ± SE of 3 independent experiments. Values marked with different letters (a, b) are significantly different from each other (P<0.05). (C) A proposed model. The Nox generates more H₂O₂ in Reoxy than in Norm, and the H₂O₂ facilitates Irs2b mediated Erk1/2 activation to induce catch-up growth. Thus the Irs2b serves as a downstream effector of re-oxygenation-induced H₂O₂. Since the excess H₂O₂ is insufficient for the significant growth acceleration in the Norm condition, other hypothetical factors (X, Y, Z, in this model) collaborating with the H₂O₂-Irs2b-Erk1/2 signaling would be involved in this catch-up growth model.