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首页> 外文期刊>American Journal of Physiology >An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts.
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An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts.

机译：拉伸对大鼠心室成纤维细胞IGF-I分泌的影响分析。

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Mechanical force can induce a number of fundamental short- and long-term responses in myocardium. These include alterations in ECM, activation of cell-signaling pathways, altered gene regulation, changes in cell proliferation and growth, and secretion of a number of peptides and growth factors. It is now known that a number of these autocrine/paracrine factors are secreted from both cardiomyocytes and ventricular cardiac fibroblasts (CFb) in response to stretch. One such substance is IGF-I. IGF-I is an important autocrine/paracrine factor that can regulate physiological or pathophysiological responses, such as hypertrophy. In this study, we addressed the possible effects of mechanical perturbation, biaxial strain, on IGF-I secretion from adult rat CFb. CFb were subjected to either static stretch (3-10%) or cyclic stretch (10%; 0.1-1 Hz) over a 24-h period. IGF-1 secretion from CFb in response to selected stretch paradigms was examined using ELISA to measure IGF-I concentrations in conditioned media. Static stretch did not result in any measurable modulation of IGF-I secretion from CFb. However, cyclic stretch significantly increased IGF-I secretion from CFb in a frequency- and time-dependent manner compared with nonstretched controls. This stretch-induced increase in secretion was relatively insensitive to changes in extracellular [Ca(2+)] or to block of L-type Ca(2+) channels. In contrast, thapsigargin, an inhibitor of sarco(endo)plasmic reticulum Ca(2+) ATPase, remarkably decreased stretch-induced IGF-I secretion from CFb. We further show that IGF-I can upregulate mRNA expression of atrial natriuretic peptide in myocytes. In summary, cyclic stretch can significantly increase IGF-I secretion from CFb, and this effect is dependent on a thapsigargin-sensitive pool of intracellular [Ca(2+)].
机译：机械力可以在心肌中引起许多基本的短期和长期反应。这些包括ECM的改变，细胞信号通路的激活，基因调控的改变，细胞增殖和生长的改变以及许多肽和生长因子的分泌。现已知道，响应舒展，心肌细胞和心室成纤维细胞（CFb）都会分泌许多这些自分泌/旁分泌因子。一种这样的物质是IGF-I。 IGF-1是一种重要的自分泌/旁分泌因子，可以调节生理或病理生理反应，例如肥大。在这项研究中，我们研究了机械扰动，双轴应变对成年大鼠CFb分泌IGF-I的可能影响。 CFb在24小时内经受了静态拉伸（3-10％）或循环拉伸（10％; 0.1-1 Hz）。使用ELISA检测条件培养基中IGF-1的浓度，检查CFb响应选定的拉伸范例而分泌的IGF-1。静态拉伸不会导致CFb对IGF-I分泌的任何可测量的调节。然而，与未拉伸的对照相比，循环拉伸以频率和时间依赖性方式显着增加了CFb的IGF-I分泌。这种拉伸诱导的分泌增加是相对不敏感的细胞外[Ca（2+）]的变化或对L型Ca（2+）通道的封锁。相比之下，thapsigargin，肌质网Ca（2+）ATPase的抑制剂，显着降低了CFb的拉伸诱导型IGF-I分泌。我们进一步表明，IGF-I可以上调心肌细胞中心钠素的mRNA表达。总之，周期性拉伸可以显着增加CFb的IGF-I分泌，这种作用取决于细胞内[Ca（2+）]的毒胡萝卜素敏感池。

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