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首页> 外文期刊>Growth hormone and IGF research: Official journal of the Growth Hormone Research Society and the International IGF Research Society >Growth hormone facilitates 5 '-azacytidine-induced myogenic but inhibits 5 '-azacytidine-induced adipogenic commitment in C3H10T1/2 mesenchymal stem cells
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Growth hormone facilitates 5 '-azacytidine-induced myogenic but inhibits 5 '-azacytidine-induced adipogenic commitment in C3H10T1/2 mesenchymal stem cells

机译：生长激素有助于5' - 碱糖苷诱导的肌原素，但抑制5' - 在C3H10T1 / 2间充质干细胞中抑制5'Azacytidine诱导的脂肪生成承诺

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摘要

The C3H10T1/2 cells are considered mesenchymal stem cells (MSCs) because they can be induced to become the progenitor cells for myocytes, adipocytes, osteoblasts, and chondrocytes by the DNA methyltransferase inhibitor 5'-azacytidine. In this study, we determined the effect of growth hormone (GH) on the myogenic and adipogenic lineage commitment in C3H10T1/2 cells. The C3H10T1/2 cells were treated with recombinant bovine GH in the presence or absence of 5'-azacytidine for 4 days. The myogenic commitment in C3H10T1/2 cells was assessed by immunostaining them for MyoD, the marker for myoblasts, and by determining their capacity to differentiate into the multinucleated myotubes. The adipogenic commitment in C3H10T1/2 cells was assessed by determining their ability to differentiate into adipocytes. Myotubes and adipocytes were identified by immunocytochemistry and Oil Red O staining, respectively. C3H10T1/2 cells treated with 5'-azacytidine and GH for 4 days contained a greater percentage of MyoD-positive cells than those treated with 5'-axacytidine alone (P 0.05). The former generated more myotubes than the latter upon induced myoblast differentiation (P 0.05). However, C3H10T1/2 cells treated with GH alone did not form any myotubes. C3H10T1/2 cells treated with 5'-azacytidine formed adipocytes upon adipocyte differentiation induction, whereas C3H10T1/2 cells treated with GH alone did not form any adipocytes. C3H10T1/2 cells treated with both 5'-azacytidine and GH formed fewer adipocytes than those treated with 5'-azacytidine alone (P 0.05). Both GHR and IGF-I mRNA expression in C3H10T1/2 cells were increased by 5'-azacytidine (P 0.05), but neither was affected by GH. Overall, this study showed that GH enhanced 5'-azacytidine-induced commitment in C3H10T1/2 cells to myoblasts but inhibited 5'-azacytidine-induced commitment to preadipocytes. These results support the possibility that GH stimulates skeletal muscle growth and inhibits adipose tissue growth in part by stimulating the myogenic commitment and inhibiting the adipogenic commitment, respectively, in mesenchymal stem cells.
机译：C3H10T1 / 2细胞被认为是间充质干细胞（MSCs），因为它们可以被DNA甲基转移酶抑制剂5'-氮杂氨酰胺成为肌细胞，脂肪细胞，成骨细胞和软骨细胞的祖细胞。在这项研究中，我们确定了生长激素（GH）对C3H10T1 / 2细胞中的肌原和脂肪性谱系承诺的影响。将C3H10T1 / 2细胞用重组牛GH处理在5'-氮杂齐乙啶的存在或不存在4天。通过将其免疫染色的MyoOD，肌细胞的标记物，并通过确定它们分化为多核肌管的能力来评估C3H10T1 / 2细胞中的肌遗传学。通过确定分化为脂肪细胞的能力来评估C3H10T1 / 2细胞中的脂肪发生承诺。通过免疫细胞化学和油红O染色分别鉴定了肌管和脂肪细胞。用5'-氮杂胞苷和GH处理的C3H10T1 / 2细胞4天含有比用5'-轴胞苷（P <0.05）处理的那些更大的MyOP阳性细胞百分比。前者在诱导肌细胞分化时产生比后者更多的myotubes（p <0.05）。然而，单独用GH处理的C3H10T1 / 2细胞未形成任何肌管。用5'-氮杂胞苷处理的C3H10T1 / 2细胞在脂肪细胞分化诱导上形成脂肪细胞，而单独使用GH处理的C3H10T1 / 2细胞未形成任何脂肪细胞。用5'-氮杂胞苷和GH处理的C3H10T1 / 2细胞比单独用5'-氮杂氨乙胺处理的脂肪细胞形成少于脂肪细胞（P <0.05）。 C3H10T1 / 2细胞中的GHR和IGF-I mRNA表达均由5'-氮杂胞苷（P <0.05）增加，但既不受GH的影响。总体而言，这项研究表明，GH增强了5'-氮杂胞苷诱导的C3H10T1 / 2细胞对肌细胞的承诺，但抑制了对前脂肪细胞的5'-氮杂胞苷诱导的承诺。这些结果支持GH刺激骨骼肌生长的可能性，并且通过刺激肌原致原因和抑制间充质干细胞抑制脂肪原承诺，抑制脂肪组织生长。

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