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首页> 外文期刊>American Journal of Physiology >Smooth muscle overexpression of IGF-I induces a novel adaptive response to small bowel resection.
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Smooth muscle overexpression of IGF-I induces a novel adaptive response to small bowel resection.

机译：IGF-I的平滑肌过度表达诱导了对小肠切除的新型适应性反应。

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摘要

Prior studies of intestinal adaptation after massive small bowel resection (SBR) have focused on growth factors and their effects on amplification of the gut mucosa. Because adaptive changes have also been described in intestinal smooth muscle, we sought to determine the effect of targeted smooth muscle growth factor overexpression on resection-induced intestinal adaptation. Male transgenic mice with smooth muscle cell overexpression of insulin-like growth factor I (IGF-I) by virtue of an alpha-smooth muscle actin promoter were obtained. SMP8 IGF-I transgenic (IGF-I TG) and nontransgenic (NT) littermates underwent 50% proximal SBR or sham operation and were then killed after 3 or 28 days. NT mice showed the expected alterations in mucosal adaptive parameters after SBR, such as increased wet weight and villus height. The IGF-I TG mice had inherently taller villi, which did not increase significantly after SBR. In addition, IGF-I TG mice had a 50% postresection persistent increase in remnant intestinal length, which was associated with an early decline and later increase in relative mucosal surface area. These results indicate that growth factor overexpression within the muscularis layer of the bowel wall induces significant postresection adaptive intestinal lengthening and a unique mucosal response. IGF-I signaling within the muscle wall may play an important role in the pathogenesis of resection-induced adaptation.
机译：小肠大肠切除术（SBR）后肠道适应的先前研究集中于生长因子及其对肠粘膜放大的影响。因为在肠道平滑肌中也已经描述了适应性变化，所以我们试图确定靶向性平滑肌生长因子过表达对切除诱导的肠道适应性的影响。获得了通过α-平滑肌肌动蛋白启动子具有胰岛素样生长因子I（IGF-1）的平滑肌细胞过表达的雄性转基因小鼠。 SMP8 IGF-I转基因（IGF-I TG）和非转基因（NT）同窝仔接受50％的近端SBR或假手术，然后在3或28天后杀死。 NT小鼠在SBR后表现出粘膜适应性参数的预期变化，例如湿重和绒毛高度增加。 IGF-I TG小鼠固有具有较高的绒毛，在SBR后并未明显增加。此外，IGF-I TG小鼠切除后残余肠长度持续增加50％，这与相对黏膜表面积的早期下降和后期增加有关。这些结果表明，肠壁肌层内的生长因子过度表达引起明显的切除后适应性肠延长和独特的粘膜反应。肌壁内的IGF-I信号传导可能在切除诱导的适应性发病机制中起重要作用。

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