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M2 muscarinic receptor activation inhibits cell proliferation and migration of rat adipose‐mesenchymal stem cells

机译:M2毒蕈碱的受体激活细胞抑制老鼠的增殖和迁移脂肪间充质干细胞

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摘要

Mesenchymal stem cells (MSCs), also known as stromal mesenchymal stem cells, are multipotent cells, which can be found in many tissues and organs as bone marrow, adipose tissue and other tissues. In particular MSCs derived from Adipose tissue (ADSCs) are the most frequently used in regenerative medicine because they are easy to source, rapidly expandable in culture and excellent differentiation potential into adipocytes, chondrocytes, and other cell types. Acetylcholine (ACh), the most important neurotransmitter in Central nervous system (CNS) and peripheral nervous system (PNS), plays important roles also in non‐neural tissue, but its functions in MSCs are still not investigated. Although MSCs express muscarinic receptor subtypes, their role is completely unknown. In the present work muscarinic cholinergic effects were characterized in rat ADSCs. Analysis by RT‐PCR demonstrates that ADSCs express M1‐M4 muscarinic receptor subtypes, whereas M2 is one of the most expressed subtype. For this reason, our attention was focused on M2 subtype. By using the selective M2 against Arecaidine Propargyl Ester (APE) we performed cell proliferation and migration assays demonstrating that APE causes cell growth and migration inhibition without affecting cell survival. Our results indicate that ACh via M2 receptors, may contribute to the maintaining of the ADSCs quiescent status. These data are the first evidence that ACh, via muscarinic receptors, might contribute to control ADSCs physiology.
机译:间充质干细胞(msc),也被称为基质间充质干细胞,是多功能的细胞,可以在许多组织和发现器官和骨髓、脂肪组织等组织。组织(ADSCs)是最常用的再生医学,因为他们很容易源,在文化和迅速扩展优秀的分化潜能为脂肪细胞、软骨细胞和其他细胞类型。乙酰胆碱(ACh),最重要的神经递质在中枢神经系统(CNS)和周围神经系统(pn)、戏剧也非神经组织应承担的重要角色,但是其功能在msc还没有调查。尽管msc表达毒蕈碱的受体子类型,他们的角色是完全未知的。目前的工作毒蕈碱的胆碱能的影响在鼠ADSCs特征。RT PCR表明应承担ADSCs表达M1 M4毒蕈碱的受体亚型,而M2是其中之一最表达亚型。我们的注意力是集中在M2亚型。选择性M2对Arecaidine炔丙基酯(猿)细胞增殖和执行迁移化验证明猿的原因抑制细胞生长和迁移影响细胞的生存。空调采暖通过M2受体,可能导致的维护的ADSCs静止状态。数据的第一个证据,通过毒蕈碱的受体,可能导致控制ADSCs生理机能。

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