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首页> 外文期刊>Cell biology international. >Low-serum culture system improves the adipogenic ability of visceral adipose tissue-derived stromal cells.
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Low-serum culture system improves the adipogenic ability of visceral adipose tissue-derived stromal cells.

机译：低血清培养系统可提高内脏脂肪组织来源的基质细胞的成脂能力。

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In obese adipose tissue, infiltrating macrophages release proinflammatory cytokines that trigger insulin resistance. An adipocyte-based platform from visceral fat would be useful to elucidate the pathology of adipose inflammation and to develop therapeutic drugs for insulin resistance. ADSCs (adipose tissue-derived mesenchymal stromal cells) expanded from subcutaneous fat are intensively studied as sources for regenerative medicine. However, the adipocyte culture system from visceral fat tissue has not been utilized yet. We aimed to establish the bioactive adipocyte platform using ADSCs from visceral fat pad. Stromal vascular fractions were processed from epididymal fat pads of Sprague-Dawley rats and three human omental fat pads, and the ADSCs were expanded using a low-serum culture method. The responses of ADSCs and ADSC-adipocytes (their adipogenic lineages) to pioglitazone, a therapeutic drug for diabesity, were evaluated by gene expression and ELISA. ADSCs (1x108) were expanded from 10 g of rat epididymal fat pads or human omental fat pads over five passages. Cell surface marker expressions revealed that visceral ADSCs were equivalent to mesenchymal stem cells. ADSC-adipocytes expanded in the low-serum culture system significantly showed higher expression of adipogenic markers [PPAR (peroxisome proliferator-activated receptor) gamma, LPL (lipoprotein lipase) and FABP4 (fatty acid-binding protein 4)] and adipocytokines [adiponectin, resistin, leptin, PAI-1 (plasminogen-activator inhibitor 1) and IL (interleukin)-10] than those expanded in a high-serum culture system. Pioglitazone accelerated the adipogenic induction and increased adiponectin expression in human ADSCs by 57.9+/-5.8-fold (mean+/-S.E.M.) relative to control cells (P<0.001). Both in rat and human ADSC-adipocytes, TNF-alpha significantly induced proinflammatory cytokines [MCP-1 (monocyte chemoattractant protein-1) and IL-6] and suppressed adiponectin expression, while pioglitazone antagonized these effects. The present findings suggest that visceral ADSC-adipocytes expanded in low-serum culture would be useful for adiposcience and pharmacological evaluations.
机译：在肥胖的脂肪组织中，浸润的巨噬细胞会释放促胰岛素抵抗的促炎细胞因子。来自内脏脂肪的基于脂肪细胞的平台将有助于阐明脂肪炎症的病理学，并开发用于胰岛素抵抗的治疗药物。从皮下脂肪中扩增出来的ADSC（脂肪组织源性间充质基质细胞）作为再生医学的来源已得到广泛研究。但是，尚未利用内脏脂肪组织的脂肪细胞培养系统。我们旨在使用内脏脂肪垫的ADSC建立具有生物活性的脂肪细胞平台。从Sprague-Dawley大鼠的附睾脂肪垫和三个人网膜脂肪垫中提取间质血管级分，并使用低血清培养方法扩增ADSC。通过基因表达和ELISA评估了ADSC和ADSC-脂肪细胞（其成脂谱系）对吡格列酮（一种用于糖尿病的治疗药物）的反应。从10克大鼠附睾脂肪垫或人网膜脂肪垫中扩增ADSC（1x108），历时五代。细胞表面标志物表达表明内脏ADSC与间充质干细胞相同。在低血清培养系统中扩增的ADSC脂肪细胞显着表达了更高的脂肪形成标记[PPAR（过氧化物酶体增殖物激活受体）γ，LPL（脂蛋白脂肪酶）和FABP4（脂肪酸结合蛋白4）]和脂肪细胞因子[adiponectin，抵抗素，瘦素，PAI-1（纤溶酶原激活物抑制剂1）和白介素（白介素-10）比在高血清培养系统中扩增的那些更强。吡格列酮使人ADSC中的脂肪形成诱导加速，脂联素表达相对于对照细胞增加了57.9 +/- 5.8倍（平均+/- S.E.M。）（P <0.001）。在大鼠和人类ADSC脂肪细胞中，TNF-α均可显着诱导促炎细胞因子[MCP-1（单核细胞趋化蛋白-1）和IL-6]，并抑制脂联素的表达，而吡格列酮则拮抗这些作用。本研究结果表明，在低血清培养物中扩增的内脏ADSC脂肪细胞将对肥胖科学和药理学评估有用。

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