Neuron-specific Mafb knockout causes growth retardationaccompanied by an impaired growth hormone/insulin-like growth factor Iaxis

摘要

Mammalian postnatal growth is regulated primarily by the growth hormone (GH)/insulin-likegrowth factor I (IGF-I) axis. MafB is a basic leucine zipper (bZip) transcription factorthat has pleiotropic functions. Although MafB plays a critical role in fetal braindevelopment, such as in guidance for hindbrain segmentation, its postnatal role in neuronsremains to be elucidated. To investigate this, we used neuron-specific conditional knockout (cKO) mice. In addition to an approximately50% neonatal viability, the cKO mice exhibited growth retardationwithout apparent signs of low energy intake. Notably, serum IGF-I levels of these mice inthe postnatal stage were lower than those of control mice. They seemed to have aneuroendocrine dysregulation, as shown by the upregulation of serum GH levels in theresting state and an inconsistent secretory response of GH upon administration of growthhormone-releasing hormone. These findings reveal that neuronal MafB plays an importantrole in postnatal development regulated by the GH/IGF-I axis.