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Early responses of the left ventricle to pressure overload in Wistar rats

机译：Wistar大鼠左心室对压力超负荷的早期反应

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The early events leading to the establishment of left ventricular hypertrophy associated to pressure overload (PO) are not well characterized. To explore these early events, aortic banding (AB) was performed in rats to induce left ventricle (LV) PO. Animals were sacrificed after 24, 48 h or 14 days. An echocardiogram was performed before the procedure and at sacrifice. LVs were preserved for the evaluation of fibrosis, angiotensin II (AT) receptors expression and stress-related MAP kinases (ERK 1/2, JNK and p38) pathways. We observed that concentric LV hypertrophy was established after only 14 days. Collagen I and fibronectin gene expressions were decreased the first 2 days after AB induction whereas AT receptors mRNA levels were sharply increased. ERK 1/2 and JNK activities in LV homogenates were decreased 24 h after AB but came back to normal after 14 days. p38 activity however was stable during the period studied. We also evaluated the presence of two phosphorylated transcription factors related to JNK signaling pathway (ATF-2 and c-Jun) in cardiomyocyte nuclei. The proportion of LV cell nuclei positive for these two activated transcription factors was significantly reduced in AB rats compared to sham. These results suggest that the early response of the LV to acute PO is to attenuate the expression of some pro-fibrotic and pro-hypertrophic signaling pathways and possibly AT signaling by decreasing ERK 1/2 and JNK relative activities. (C) 2007 Elsevier Inc. All rights reserved.
机译：导致与压力超负荷（PO）相关的左心室肥大的早期事件尚未得到很好的表征。为了探索这些早期事件，在大鼠中进行了主动脉束带（AB）诱导左心室（LV）PO。 24、48小时或14天后处死动物。在手术前和处死时进行超声心动图检查。保留LV用于评估纤维化，血管紧张素II（AT）受体表达和与压力相关的MAP激酶（ERK 1/2，JNK和p38）途径。我们观察到仅14天就建立了同心LV肥大。 AB诱导后的前两天，胶原蛋白I和纤连蛋白基因表达降低，而AT受体mRNA水平急剧升高。 AB后24小时，LV匀浆中的ERK 1/2和JNK活性降低，但14天后恢复正常。然而，在研究期间p38活性是稳定的。我们还评估了心肌细胞核中与JNK信号通路（ATF-2和c-Jun）相关的两个磷酸化转录因子的存在。与假手术相比，AB大鼠中这两个激活的转录因子阳性的LV细胞核比例显着降低。这些结果表明LV对急性PO的早期反应是通过降低ERK 1/2和JNK的相对活性来减弱某些促纤维化和促肥大信号通路的表达，并可能减弱AT信号通路的表达。 （C）2007 Elsevier Inc.保留所有权利。

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