A new function of Nell-1 protein in repressing adipogenic differentiation.
A new function of Nell-1 protein in repressing adipogenic differentiation.
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DOI：
10.1016/j.bbrc.2011.06.111
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发表时间：
2011-07-22
影响因子：
3.1
通讯作者：
Soo, Chia
中科院分区：
文献类型：
--
作者：
James, Aaron W.;Pan, Angel;Chiang, Michael;Zara, Janette N.;Zhang, Xinli;Ting, Kang;Soo, Chia
长期以来，人们一直假设成骨和脂肪分化（骨与脂肪组织分化）存在理论上的反比关系。理论上，这种反比关系至少部分地构成了骨质疏松症的临床实体，其中骨髓间充质干细胞（MSC）具有随着年龄的增长而增加的脂肪分化倾向。在本研究中，我们测定了 Nell-1 蛋白（一种骨诱导分子）的潜在抗脂肪作用。使用 3T3-L1（人前脂肪细胞系）细胞和人脂肪源性基质细胞 (ASC)，我们观察到腺病毒递送的 (Ad)-Nell-1 或重组 NELL-1 蛋白显着降低了所有检查标记物的脂肪分化（油红 O 染色、脂肪形成基因表达 [Pparg、Lpl、Ap2]）。以前瞻性的方式，Hedgehog 信号被分析为 Nell-1 信号在调节成骨分化和成脂分化方面的潜在下游。与 Ad-LacZ 对照相比，Ad-Nell-1 增加了刺猬信号标记（Ihh、Gli1、Ptc1）的表达。这些研究表明 Nell-1 是一种有效的抗脂肪形成剂。此外，Nell-1 信号传导可能通过 Hedgehog 依赖性机制抑制脂肪形成分化。
A theoretical inverse relationship has long been postulated for osteogenic and adipogenic differentiation (bone versus adipose tissue differentiation). This inverse relationship in theory at least partially underlies the clinical entity of osteoporosis, in which marrow mesenchymal stem cells (MSCs) have a predilection for adipose differentiation that increases with age. In the present study, we assayed the potential anti-adipogenic effects of Nell-1 protein (an osteoinductive molecule). Using 3T3-L1 (a human preadipocyte cell line) cells and human adipose-derived stromal cells (ASCs), we observed that adenoviral delivered (Ad)-Nell-1 or recombinant NELL-1 protein significantly reduced adipose differentiation across all markers examined (Oil red O staining, adipogenic gene expression [Pparg, Lpl, Ap2]). In a prospective fashion, Hedgehog signaling was assayed as potentially downstream of Nell-1 signaling in regulating osteogenic over adipogenic differentiation. In comparison to Ad-LacZ control, Ad-Nell-1 increased expression of hedgehog signaling markers (Ihh, Gli1, Ptc1). These studies suggest that Nell-1 is a potent anti-adipogenic agent. Moreover, Nell-1 signaling may inhibit adipogenic differentiation via a Hedgehog dependent mechanism.
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影响因子：
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作者：
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通讯作者：
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影响因子：
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