Literature DB >> 16139964

Dysfunction of releasing adrenaline in asthma by nerve growth factor.

Jun Tao Feng1, Cheng Ping Hu.   

Abstract

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 well 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 unpuzzle 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.

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Year:  2005        PMID: 16139964     DOI: 10.1016/j.mehy.2005.06.029

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  5 in total

1.  Kidney-tonifying recipe can repair alterations in adrenal medullary chromaffin cells in asthmatic rats.

Authors:  Cheng-Ping Hu; Jun-Tao Zou; Ye-Qiang Zou; Xiao-Zhao Li; Jun-Tao Feng
Journal:  Evid Based Complement Alternat Med       Date:  2012-03-11       Impact factor: 2.629

2.  Asthma pregnancy alters postnatal development of chromaffin cells in the rat adrenal medulla.

Authors:  Xiu-Ming Wu; Cheng-Ping Hu; Xiao-Zhao Li; Ye-Qiang Zou; Jun-Tao Zou; Yuan-Yuan Li; Jun-Tao Feng
Journal:  PLoS One       Date:  2011-05-27       Impact factor: 3.240

3.  Redistribution of adrenomedullary nicotinic acetylcholine receptor subunits and the effect on circulating epinephrine levels in a murine model of acute asthma.

Authors:  Xi Chen; Juntao Feng; Chengping Hu; Qingwu Qin; Yuanyuan Li; Ling Qin
Journal:  Int J Mol Med       Date:  2016-12-23       Impact factor: 4.101

4.  The effect of unilateral adrenalectomy on transformation of adrenal medullary chromaffin cells in vivo: a potential mechanism of asthma pathogenesis.

Authors:  Cheng-Ping Hu; Ye-Qiang Zou; Jun-Tao Feng; Xiao-Zhao Li
Journal:  PLoS One       Date:  2012-09-05       Impact factor: 3.240

5.  Transformation of adrenal medullary chromaffin cells increases asthmatic susceptibility in pups from allergen-sensitized rats.

Authors:  Jun-Tao Feng; Xiu-Ming Wu; Xiao-Zhao Li; Ye-Qiang Zou; Ling Qin; Cheng-Ping Hu
Journal:  Respir Res       Date:  2012-11-08
  5 in total

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