Fad104, a positive regulator of adipogenesis, negatively regulates osteoblast differentiation
Fad104, a positive regulator of adipogenesis, negatively regulates osteoblast differentiation
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DOI：
10.1016/j.bbrc.2010.05.077
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发表时间：
2010-06-25
影响因子：
3.1
通讯作者：
Imagawa, Masayoshi
中科院分区：
文献类型：
--
作者：
Kishimoto, Keishi;Kato, Ayumi;Imagawa, Masayoshi
脂肪细胞分化因子（Fad104）是一个在脂肪细胞分化早期临时表达的新基因。之前，我们发现fad104促进小鼠31341细胞和小鼠胚胎成纤维细胞（mef）的脂肪细胞分化。此外，我们报道了植入的野生型mef可以发育成脂肪细胞，而fad104缺陷的mef则不能。有趣的是，骨样组织仅在fad - 104缺失mef的植入物中观察到。这一结果提示fad104参与成骨细胞分化。然而，fad104在成骨过程中的功能尚不清楚。在本文中，我们发现fad 104负向调控成骨细胞分化。在分化过程中，fad104表达水平下降。fad104的缺失促进了mef中成骨细胞的分化，并提高了成骨细胞分化的主要调控因子runx2的水平。fad104的破坏抑制了MEFs中bmp -2介导的脂肪细胞分化。总之，我们证明fad104相互调节脂肪细胞和成骨细胞的分化；在脂肪细胞分化中起正调节作用，在成骨细胞分化中起负调节作用。(C) 2010爱思唯尔公司版权所有。
Fad104 (factor for adipocyte differentiation 104) is a novel gene expressed temporarily in the early stages of adipocyte differentiation. Previously, we showed that fad104 promotes adipocyte differentiation in mouse 31341 cells and mouse embryonic fibroblasts (MEFs). Furthermore, we reported that implanted wild-type MEFs could develop into adipocytes, whereas fad104-deficient MEFs could not. Interestingly, bone-like tissues were only observed in the implants derived from fad 104-deficient MEFs. This result implies that fad104 is involved in osteoblast differentiation. However, the functions of fad104 during osteogenesis are unknown. In this paper, we show that fad 104 negatively regulates osteoblast differentiation. During the differentiation process, the level of fad104 expression decreased. Deletion of fad104 facilitated osteoblast differentiation in MEFs, and elevated the level of runx2, a master regulator of osteoblast differentiation. Disruption of fad104 suppressed BMP-2-mediated adipocyte differentiation in MEFs. In conclusion, we demonstrate that fad104 reciprocally regulates differentiation of adipocytes and osteoblast; functions as a positive regulator in adipocyte differentiation and as a negative regulator in osteoblast differentiation. (C) 2010 Elsevier Inc. All rights reserved.