Turnley Ann M
Centre for Neuroscience, The University of Melbourne, Victoria, Australia.
Pediatr Endocrinol Rev. 2005 Mar;2(3):366-71.
Although many overgrowth and growth deficient patients have apparently normal neuropsychological and cognitive functions, there is evidence to suggest that in some instances these functions are somewhat impaired. Altered growth hormone (GH) signaling is primarily responsible for many growth phenotypes and its signaling is regulated by a number of molecules, including members of the suppressor of cytokine signaling (SOCS) family, in particular SOCS2. GH and SOCS2 have recently been shown to regulate neuronal differentiation by controlling expression of a neurogenic transcription factor, Neurogenin-1. Furthermore, SOCS2 regulates neurite outgrowth from neurons. Together, GH and SOCS2 play a role in regulating the numbers and types of neurons formed during development, as well as the connections they make in the central nervous system. This review will explore the possibility that an alteration in the balance of GH and SOCS2 may therefore lead to neural defects and some possible mechanisms will be examined.
尽管许多生长过度和生长缺陷的患者具有明显正常的神经心理和认知功能，但有证据表明，在某些情况下，这些功能会受到一定程度的损害。生长激素（GH）信号改变是许多生长表型的主要原因，其信号由多种分子调节，包括细胞因子信号抑制因子（SOCS）家族成员，特别是SOCS2。最近研究表明，GH和SOCS2通过控制神经源性转录因子Neurogenin-1的表达来调节神经元分化。此外，SOCS2调节神经元的轴突生长。GH和SOCS2共同作用，在调节发育过程中形成的神经元数量和类型以及它们在中枢神经系统中的连接方面发挥作用。本综述将探讨GH和SOCS2平衡改变可能导致神经缺陷的可能性，并研究一些可能的机制。
