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首页> 外文期刊>Life sciences >Long-term induction of beta-CGRP mRNA in rat lungs by allergic inflammation.
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Long-term induction of beta-CGRP mRNA in rat lungs by allergic inflammation.

机译：过敏性炎症可长期诱导大鼠肺中β-CGRPmRNA的表达。

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Calcitonin gene-related peptide (CGRP) is one of the major neuropeptides released from sensory nerve endings and neuroendocrine cells of the lung. Two CGRP isoforms, alpha-and beta-CGRP, have been identified in rats and humans, but no studies have attempted to reveal direct evidence of differences in action or location of these isoforms in allergic inflammation (AI). We investigated mRNA expressions of alpha-and beta-CGRP in lungs, nodose ganglia (NG), and dorsal root ganglia (DRG) of an animal model for AI of the airways, utilizing a model created by sensitizing Brown Norway (BN) rats with ovalbumin (OVA). By semiquantitative RT-PCR analysis, long-lasting enhanced expression of the beta-CGRP mRNA was shown in the lungs of the AI rats (14.5-fold enhancement at 6 hr, 8.1-fold at 24 hr, and 3.7-fold at 120 hr after OVA-challenge compared to the level in the lungs of phosphate-buffered saline (PBS)-challenged control rats). In contrast, the mRNA expression of the alpha-CGRP in AI lungs showed only a transient increase after OVA-challenge (2.7-fold at 6 hr) followed by a lower level of expression (0.5-fold at 48 hr and 0.6-fold at 120 hr). The mRNA expressions of both isoforms in NG, but not in DRG, were transiently up-regulated at 6 hr after antigen challenge. In situ RT-PCR in combination with immunohistochemical analysis revealed that beta-CGRP was expressed in neuroendocrine cells in clusters (termed neuroepithelial bodies [NEBs]) in AI lungs. These results indicate that the long-term induction of beta-CGRP in NEBs may play an important role in pulmonary AI such as bronchial asthma.
机译：降钙素基因相关肽（CGRP）是从肺的感觉神经末梢和神经内分泌细胞释放的主要神经肽之一。在大鼠和人类中已鉴定出两种CGRP亚型，即α-和β-CGRP，但尚无研究试图揭示这些亚型在变应性炎症（AI）中作用或位置差异的直接证据。我们使用通过使褐挪威（BN）大鼠致敏的模型建立的模型，研究了气道AI动物模型的肺，结节神经节（NG）和背根神经节（DRG）中的α和β-CGRP的mRNA表达。卵清蛋白（OVA）。通过半定量RT-PCR分析，在AI大鼠的肺中显示了β-CGRPmRNA的持久增强表达（6小时增强了14.5倍，24小时增强了8.1倍，120小时增强了3.7倍） OVA攻击后的水平与磷酸盐缓冲盐水（PBS）挑战的对照组大鼠的肺水平相比）。相比之下，AI肺中α-CGRP的mRNA表达仅在OVA攻击后短暂增加（6小时时为2.7倍），随后表达水平较低（48小时时为0.5倍，而0.6小时时为0.6倍） 120小时）。在抗原攻击后6小时，NG中的两种同工型的mRNA表达都被上调，而DRG中的两种同工型的mRNA表达却被瞬时上调。原位RT-PCR结合免疫组织化学分析显示，β-CGRP在AI肺的簇（称为神经上皮体[NEBs]）的神经内分泌细胞中表达。这些结果表明，NEB中长期诱导β-CGRP可能在支气管哮喘等肺部AI中起重要作用。

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