Dysfunction of releasing adrenaline in asthma by nerve growth factor
Dysfunction of releasing adrenaline in asthma by nerve growth factor
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DOI：
10.1016/j.mehy.2005.06.029
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发表时间：
2005-01-01
影响因子：
4.7
通讯作者：
Hu, CP
中科院分区：
文献类型：
--
作者：
Feng, JT;Hu, CP
在胚胎早期，肾上腺髓质的发育与肾上腺素能神经的发育是平行的。因此，肾上腺髓质细胞可能具有向神经细胞转分化的潜在能力。体外实验充分证明，肾上腺髓质细胞经神经生长因子处理后，可向具有形态、生化和生理功能特征的交感神经元转分化。导致转分化后的肾上腺髓质细胞内分泌功能受损，肾上腺髓质激素的组成和水平发生改变。上述可以看作是细胞冗余的体现，除了转分化之外，细胞器的多拷贝、细胞可塑性等都是细胞冗余的体现。根据细胞冗余性，某些细胞（类型）除了其常规和特定功能外，还具有其他附加功能，这些功能在疾病、外部干扰等特殊状态下会被激活。细胞冗余理论似乎解开了哮喘中肾上腺素释放功能障碍的谜团。研究表明，与正常对照组相比，哮喘患者的肾上腺素水平在遇到强烈刺激时并未升高。随后，在哮喘患者和动物中也检测到神经生长因子的过度表达。然而，随着气道炎症的缓解，当用神经生长因子抗体治疗哮喘模型时，这些现象发生了改变。是什么让这些现象相互关联？髓细胞功能冗余的存在可能是最重要的因素。这一假设表明，神经生长因子的过度表达激活肾上腺髓质细胞的功能冗余，从而使这些细胞向交感神经元转分化。转分化（倾向）可能损害肾上腺髓质细胞的内分泌功能。结果，肾上腺髓质无法释放足够的肾上腺素来缓解哮喘发作时的支气管收缩。 (c) 2005 Elsevier Ltd. 保留所有权利。
In early embryo period, adrenal medulla development is parallel with adrenergic nerves. For this reason, adrenal medullary cells may be provided with potential ability of transdifferentiation toward nerve cells. In vitro, it was welt testified that if adrenal medullary cells are treated with nerve growth factor, then the cells will be transdifferentiated toward sympathetic neurons characterized by morphous, biochemistry and physiological functions. As a result, adrenal medullary cells after being transdifferentiated may be impaired in the functions of endocrine secretion, and the composition and level of adrenal medullary hormone are changed. The above mentioned may be regarded as the reflection of cellular redundancy, besides the transdifferentiation, multiple organelle copies, cellular plasticity and so on are all reflections of cellular redundancy. According to cellular redundancy, in addition to their regular and specific functions, some cells(types) are of other additional functions which will be activated in special state such as diseases, external interference and so on. The theory of cellular redundancy is seemed to unpuzzte the dysfunction of releasing adrenaline in asthma. Compared with the normal control group, the study showed that the levels of adrenaline in the asthmatic patients were not increased when patients encountered the strong stimuli. Subsequently, overexpression of nerve growth factor was also detected in asthmatic patients and animals. However, accompanied with alleviation of airway inflammation, these phenomena were changed when asthmatic models were treated with antibody of nerve growth factor. What makes these phenomena linked? The existence of functional redundancy of medullary cells may be the most important factor. This hypothesis suggests that overexpression of nerve growth factor activate functional redundancy of adrenal medullary cells, which makes these cells transdifferentiated toward sympathetic neurons. The transdifferentiation (tendency) may impair the functions of endocrine secretion of adrenal medullary cells. As a result, adrenal medulla cannot release enough adrenaline to relieve bronchoconstriction in asthmatic attack. (c) 2005 Elsevier Ltd. All rights reserved.