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首页> 外文期刊>Hypertension research: Official journal of the Japanese Society of Hypertension >Cellular physiology of rat cardiac myocytes in cardiac fibrosis: in vitro simulation using the cardiac myocyte/cardiac non-myocyte co-culture system.
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Cellular physiology of rat cardiac myocytes in cardiac fibrosis: in vitro simulation using the cardiac myocyte/cardiac non-myocyte co-culture system.

机译：心脏纤维化中大鼠心脏心肌细胞的细胞生理学：使用心脏心肌细胞/心脏非心肌细胞共培养系统的体外模拟。

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An understanding of the cellular physiology of cardiac myocytes (MCs) and non-myocytes (NMCs) may help to explain the mechanisms underlying cardiac hypertrophy. Despite numerous studies using MC/NMC co-culture systems, it is difficult to precisely evaluate the influence of each cell type because of the inherent cellular heterogeneity of such a system. Here we developed a co-culture system using Wistar rat neonatal MCs and NMCs isolated by discontinuous Percoll gradient and adhesion separation methods and cultured on either side of insert well membranes. Co-culture of MCs and NMCs resulted in significant increases in [3H]-leucine incorporation by MCs, in the amount of protein synthesized by MCs, and in the secretion of natriuretic peptides, while the addition of MCs to NMC cultures significantly reduced [3H]-thymidine incorporation by NMCs. Interestingly, the percentage of the brain natriuretic peptide (BNP) component of total natriuretic peptide secreted (atrial natriuretic peptide+BNP) increased as the number of NMCs placed in the MC/NMC co-culture system increased. However, MCs did not affect production of angiotensin II (Ang II) by NMCs or secretion of endothelin-1 and transforming growth factor-beta1 into the MC/NMC co-culture system. This finding was supported by the anti-hypertrophic and anti-fibrotic actions of RNH6270, an active form of olmesartan, on MCs in the MC/NMC co-culture system and on NMCs that may synthesize Ang II in the heart. The present data indicate that cardiac fibrosis may not only facilitate MC hypertrophy (possibly through the local angiotensin system) but may also change particular pathophysiological properties of MCs, such as the secretory pattern of natriuretic peptides.
机译：对心肌细胞（MCs）和非心肌细胞（NMCs）的细胞生理学的理解可能有助于解释心脏肥大的机制。尽管使用MC / NMC共培养系统进行了大量研究，但由于这种系统固有的细胞异质性，因此难以精确评估每种细胞类型的影响。在这里，我们开发了一种共培养系统，该系统使用Wistar大鼠新生MC和NMC通过不连续的Percoll梯度和粘附分离方法分离，并在插入孔膜的两侧进行培养。 MC和NMC的共培养导致[3H]-亮氨酸被MC掺入，MC合成的蛋白质量以及利尿钠肽分泌的显着增加，而向NMC培养物中添加MC则显着减少了[3H] NMC将]-胸苷掺入。有趣的是，随着放置在MC / NMC共培养系统中的NMC数量的增加，分泌的总脑钠肽（脑钠肽+ BNP）中脑钠肽（BNP）成分的百分比增加。但是，MCs不会影响NMC产生血管紧张素II（Ang II）或内皮素-1的分泌并将生长因子β1转化为MC / NMC共培养系统。 RNH6270（一种有效形式的奥美沙坦）对MC / NMC共培养系统中的MC以及可能在心脏中合成Ang II的NMC的抗肥大和抗纤维化作用支持了这一发现。目前的数据表明，心脏纤维化不仅可以促进MC肥大（可能通过局部血管紧张素系统），而且可以改变MC的特定病理生理特性，例如利钠肽的分泌模式。

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