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首页> 外文期刊>The European Journal of Neuroscience >Isoform-selective as opposed to complete depletion of fibroblast growth factor 2 (FGF-2) has no major impact on survival and gene expression in SOD1(G93A) amyotrophic lateral sclerosis mice
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Isoform-selective as opposed to complete depletion of fibroblast growth factor 2 (FGF-2) has no major impact on survival and gene expression in SOD1(G93A) amyotrophic lateral sclerosis mice

机译：同种型选择性与完全耗尽成纤维细胞生长因子2（FGF-2）对SOD1（G93A）肌萎缩侧硬化小鼠的存活和基因表达没有重大影响

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摘要

We have previously shown that total knockout of fibroblast growth factor-2 (FGF-2) results in prolonged survival and improved motor performance in superoxide dismutase 1 (SOD1(G93A)) mutant mice, the most widely used animal model of the fatal adult onset motor neuron disease amyotrophic lateral sclerosis (ALS). Moreover, we found differential expression of growth factors in SOD1(G93A) mice, with distinct regulation patterns of FGF-2 in spinal cord and muscle tissue. Within the present study we aimed to characterize FGF-2-isoform specific effects on survival, motor performance as well as gene expression patterns predominantly in muscle tissue by generating double mutant SOD1(G93A)FGF-2 high molecular weight- and SOD1(G93A)FGF-2 low molecular weight-knockout mice. While isoform specific depletion was not beneficial regarding survival or motor performance of double mutant mice, we found isoform-dependent differential gene expression of epidermal growth factor (EGF) in the muscle of SOD1(G93A)FGF-2 low molecular weight knockout mice compared to single mutant SOD1(G93A) mice. This significant downregulation of EGF in the muscle tissue of double mutant SOD1(G93A)FGF-2 low molecular weight knockout mice implies that FGF-2 low molecular weight knockout (or the presence of the FGF-2 high molecular weight isoform) selectively impacts EGF gene expression in ALS muscle tissue.
机译：我们之前已经表明，成纤维细胞生长因子-2（FGF-2）的总敲除导致超氧化物歧化酶1（SOD1（G93A））突变小鼠的延长存活和改善的电动机性能，最广泛使用的致命成人发病的动物模型运动神经元疾病肌营养侧面硬化剂（ALS）。此外，我们发现SOD1（G93A）小鼠生长因子的差异表达，具有脊髓和肌肉组织中FGF-2的明显调控模式。在本研究中，我们旨在通过产生双突变体SOD1（G93A）FGF-2高分子量和SOD1（G93A）来表征对生存，电动机性能以及肌肉组织中的基因表达模式。 FGF-2低分子量敲除小鼠。虽然同种型特异性耗竭对双突变小鼠的存活或电机性能没有有益，但我们发现SOD1（G93A）FGF-2低分子量敲除小鼠的肌肉中表皮生长因子（EGF）的异形依赖性差异基因表达单突变体SOD1（G93A）小鼠。双突变体SOD1（G93A）FGF-2低分子量敲除小鼠的肌肉组织中EGF的显着下调意味着FGF-2低分子量敲除（或FGF-2高分子量同种型的存在）选择性地影响EGF在Als肌肉组织中的基因表达。

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