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. 2004 Jun 1;113(11):1535–1549. doi: 10.1172/JCI19906

Figure 9.

Figure 9

GSK-3β, and not GSK-3α, regulates the protection state. (A) SiRNA treatment specifically decreases respective protein levels of GSK-3α and GSK-3β in neonatal rat cardiac myocytes; GFP siRNA and media alone served as negative controls. Immunoblot of cell lysates probed with antibodies against GSK-3α/β, GSK-3β, and 39-kDa subunit of mitochondrial Complex I (as a loading control). The immunoblot is representative of two independent experiments. (B) Silencing of GSK-3β, but not of GSK-3α, enhances tMPT to levels comparable to insulin-induced protection in neonatal rat cardiac myocytes. Data comprise two independent experiments; n = 30 in each group (except n = 22 for GFP siRNA). *P < 0.02, **P < 0.001, ***P < 0.0001 vs. respective control. (C) Constitutive activation of GSK-3β prevents ability to engage protective signaling. GSK-3β inhibition is required for protection against oxidative stress. Both mitochondrial sweller_dependent and _independent protection mechanisms are abolished in adult cardiac myocytes from GSK-3β S9A TG mice. *P < 0.02 vs. control. (D) Hypoxic PC protection after hypoxia/reoxygenation is abolished in adult cardiac myocytes from GSK-3β S9A TG mice. #P < 0.01 vs. control.