Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Li, Q G; Wu, Xiaorong; Li, X Z; Yu, Jia-Kuo; Xia, Yixin; Wang, A P; Wang, J

doi:10.4238/2012.august.24.3

Cited by 9 publications

(6 citation statements)

References 25 publications

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“…Previous studies reported the presence of an ePi secretion disorder in asthmatic model rats, with a mechanism closely associated with nGF-induced neuronal transformation and endocrine dysfunction in aMccs (21,27). The present study hypothesized that nGF increased significantly in an ar mouse model and assessed its ability to induce the transformation of aMccs from endocrine phenotypes to neuronal cell phenotypes and then cause a decrease in ePi secretion.…”

Section: Nerve Growth Factor Causes Epinephrine Release Dysfunction B...mentioning

confidence: 83%

Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis

et al. 2023

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The presence of allergic rhinitis (ar) is an increased risk factor for the occurrence of bronchial asthma (Ba). nerve growth factor (nGF), in addition to its key role in the development and differentiation of neurons, may also be an important inflammatory factor in AR and BA. However, the pathogenesis of the progression of ar to Ba remains to be elucidated. The present study aimed to investigate the ability of nGF to mediate nasobronchial interactions and explore possible underlying molecular mechanisms. in the present study, an ar mouse model was established and histology of nasal mucosa tissue injury was determined. The level of phenylethanolamine n-methyl transferase in adrenal medulla was determined by immunofluorescence. Primary adrenal medullary chromaffin cells (aMccs) were isolated and cultured from the adrenal medulla of mice. The expression levels of synaptophysin (SYP), STaT1, JaK1, p38 and erK in nGF-treated and untreated aMccs were detected by reverse-transcription-quantitative Pcr and western blotting. The epinephrine (ePi) and norepinephrine (ne) concentrations were measured by eliSa. it was found that the expression of SYP in aMccs was enhanced in the presence of nGF, whereas, the concentration of EPI decreased significantly under the same conditions. Furthermore, nGF mediated the phenotypic and functional changes of aMccs, resulting in decreased ePi secretion via JaK1/STaT1, p38 and erK signaling. in conclusion, these findings could provide novel evidence for the role of NGF in regulating neuroendocrine mechanisms.

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Section: Nerve Growth Factor Causes Epinephrine Release Dysfunction B...mentioning

confidence: 83%

Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis

et al. 2023

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“…Asthma is an airway inflammatory disease with an underlying Th2 cell-mediated inflammatory response in the airways ( 18 ). Increased levels of NGF expression are observed in patients with asthma following bronchial provocation with an allergen, and are associated with the severity of the inflammatory process and disease ( 19 – 21 ). Furthermore, a previous study demonstrated that NGF may exacerbate allergic lung inflammation in an animal model of asthma ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

Lung dendritic cells undergo maturation and polarization towards a T helper type 2-stimulating phenotype in a mouse model of asthma: Role of nerve growth factor

Qin

Wang

Pan

et al. 2014

Experimental and Therapeutic Medicine

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Nerve growth factor (NGF) and dendritic cells (DCs) have been hypothesized to modulate T cell responses in a mouse model of asthma. However, whether NGF plays a role in regulating the maturation and polarization of lung DCs remains unclear. In the present study, the effect of NGF inhibition on the maturation and phenotype of lung DCs was investigated in a mouse model of asthma. BALB/c mice were sensitized and challenged with ovalbumin (OVA), and subsequently received anti-NGF treatment. At 24 h following the last challenge, airway responsiveness and inflammation were examined. The concentrations of NGF, interferon (IFN)-γ and interleukin (IL)-4 were analyzed. In addition, maturation and CD103 expression in the lung DCs were investigated. Anti-NGF treatment was found to significantly reduce airway hyperreactivity and inflammation in asthmatic mice. In addition, a subdued T helper 2 (Th2) response was observed, characterized by the downregulation of IL-4 and the upregulation of IFN-γ. Furthermore, the expression of the DC surface molecules, CD80, CD86 and major histocompatibility complex class II, as well as the proportion of lung CD103+ DCs, decreased in the OVA-sensitized and challenged mice. The proportion of lung CD103+ DCs also exhibited a positive correlation with the levels of plasma NGF in the mice. These results may provide an explanation for the role of NGF in amplifying the Th2 response in allergic diseases. Therefore, NGF may promote the maturation and polarization towards a Th2-stimulating phenotype of activated DCs, contributing to an amplification of the Th2 response in asthma.

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“…Similarly, mature and immature adrenal medullary cells have a pluripotent differentiation capacity in varying degrees (3,4). It has been verified by in vivo (5,6) and in vitro (3,7,8) studies that in a environment rich in NGF, adrenal medullary cells can transform from an endocrine phenotype into a neuronal one and their endocrine function simultaneously changes with the transformation.…”

Section: Introductionmentioning

confidence: 90%

Proteomic analysis of NGF-induced transdifferentiation of adrenal medullary cells

Sun

et al. 2013

International Journal of Molecular Medicine

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Nerve growth factor (NGF) is a polypeptide growth factor with specific trophic function in nerve cells and was initially investigated for its role as a key player in the regulation of peripheral innervations. The aim of this study was to examine the NGF-induced transdifferentiation of adrenal medullary cells, and to screen the major candidate differentially expressed proteins involved in the transdifferentiation. NGF was used to treat primary cultures of neonatal calf adrenal medullary cells and the effects of transdifferentiation were determined in association with cellular morphology, ultrastructure and changes in endocrine function. Differentially expressed proteins were screened and identified through two-dimensional gel electrophoresis and mass spectrometry. The protein spots showing differential expression were verified by western blot analysis. We observed neurite outgrowth in the adrenal medullary cells treated with NGF under a phase contrast microscope. Ultrastructure analysis revealed that there were rich drumstick-like and villiform processes on the cell membranes and vesicles were formed near the cell membranes. The cytoplasm was rich in mitochondria and the secretion of epinephrine was decreased. Two-dimensional gel electrophoresis revealed that among the differentially expressed proteins, 48 protein spots showed an upregulated expression and 37 protein spots showed a downregulated expression, and no 'all-or-none' spots with significant differences in expression were found. Fourteen protein spots with an upregulated expression and 6 with a downregulated expression were randomly selected for identification by mass spectrometry. Western blot analysis revealed that ras homologus oncogene (Rho) GDP dissociation inhibitor α (RhoGDIα) protein expression was significantly downregulated and peripherin protein expression was significantly upregulated. In brief, our data demonstrate that NGF can induce the differentiation of adrenal medullary cells into neurons, and that RhoGDIα and peripherin may play important roles in this process.

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Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Cited by 9 publications

References 25 publications

Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis

Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis

Lung dendritic cells undergo maturation and polarization towards a T helper type 2-stimulating phenotype in a mouse model of asthma: Role of nerve growth factor

Proteomic analysis of NGF-induced transdifferentiation of adrenal medullary cells

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