Increased Linear Bone Growth by GH in the Absence of SOCS2 is Independent of IGF-1

摘要: Growth hormone (GH) signaling is essential for postnatal linear bone growth, but the relative importance of GHs actions on liver and/or growth plate cartilage remains unclear. The derived insulin like-growth factor-1 (IGF-1) endochondral has recently been challenged. Here, we investigate in Suppressor Cytokine Signaling-2 (SOCS2) knockout mice, which have enhanced despite normal systemic GH/IGF-1 levels. Wild-type embryonic ex vivo metatarsals failed to exhibit increased response GH, displayed Socs2 transcript levels (P < 0.01). In absence SOCS2, GH treatment metatarsal over a 12 day period. Despite this increase, IGF-1 and protein were not GH. accordance with these data, unchanged GH-challenged Socs2-/- conditioned medium showing growth. Growth-plate Igf1 mRNA elevated juvenile mice. did however elevate IGF-binding 3 from challenged was more apparent metatarsals. enhance when IGF receptor inhibited, suggesting that mediated mechanisms are required. IGF-2 may be responsible as promoted Igf2 expression (but WT) These studies emphasise critical SOCS2 regulating ability promote Also, appears act directly promoting via mechanism independent IGF-1. J. Cell. Physiol. 9999: 2796–2806, 2015. © 2015 Wiley Periodicals, Inc.