Neurotrophins and target interactions in the development and regulation of sympathetic neuron electrical and synaptic properties

Luther, Jason A.; Birren, Susan J.

doi:10.1016/j.autneu.2009.08.009

Cited by 41 publications

(31 citation statements)

References 210 publications

(345 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the nervous system, growth factors called neurotrophins (NTs) are well recognized for their role in the generation, growth, and maintenance of different neuronal populations (5)(6)(7)(8)(9). Both short-term (seconds or minutes) and long-term (hours or days) effects of NTs on nuclear and cytosolic signals have been recognized as favoring increased synaptic transmission and plasticity, cell proliferation, and survival.…”

mentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Cigarette Smoke–Induced Airway Hyperreactivity

Sathish¹,

VanOosten²,

Miller³

et al. 2013

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Enhanced airway smooth muscle (ASM) contractility contributes to increased resistance to airflow in diseases such as bronchitis and asthma that occur in passive smokers exposed to secondhand smoke. Little information exists on the cellular mechanisms underlying such airway hyperreactivity. Sputum samples of patients with chronic sinusitis, bronchitis, and asthma show increased concentrations of growth factors called neurotrophins, including brain-derived growth factor (BDNF), but their physiological significance remains unknown. In human ASM, we tested the hypothesis that BDNF contributes to increased contractility with cigarette smoke exposure. The exposure of ASM to 1% or 2% cigarette smoke extract (CSE) for 24 hours increased intracellular calcium ([Ca 21 ] i ) responses to histamine, and further potentiated the enhancing effects of a range of BDNF concentrations on such histamine responses. CSE exposure increased the expression of the both high-affinity and lowaffinity neurotrophin receptors tropomyosin-related kinase (Trk)-B and p75 pan-neurotrophin receptor, respectively. Quantitative ELISA showed that CSE increased BDNF secretion by human ASM cells. BDNF small interfering (si)RNA and/or the chelation of extracellular BDNF, using TrkB-fragment crystallizable, blunted the effects of CSE on [Ca 21 ] i responses as well as the CSE enhancement of cell proliferation, whereas TrkB siRNA blunted the effects of CSE on ASM contractility. These data suggest that cigarette smoke is a potent inducer of BDNF and TrkB expression and signaling in ASM, which then contribute to cigarette smoke-induced airway hyperresponsiveness.Keywords: neurotrophin; asthma; TrkB; environmental tobacco exposure; secondhand smoke Airway diseases such as asthma and chronic obstructive pulmonary disease (COPD) can be triggered or exacerbated by cigarette smoke and secondhand smoke exposure (1-4). Furthermore, in people with preexisting airway diseases such as asthma, acute exposure to cigarette smoke can produce a bronchospastic response. Considerable evidence already exists that airway inflammation occurs with cigarette smoke exposure, and contributes to airway disease even in passive smokers. Regardless of the underlying causes for airway inflammation (of which there are many), increased airway smooth muscle (ASM) contractility is certainly a key factor contributing to the pathological airway narrowing and increased airflow resistance observed in asthma and bronchitis. Although smoke exposure is recognized to increase airway contractility, the mechanisms by which cigarette smoke enhances ASM contractility remain under investigation.In the nervous system, growth factors called neurotrophins (NTs) are well recognized for their role in the generation, growth, and maintenance of different neuronal populations (5-9). Both short-term (seconds or minutes) and long-term (hours or days) effects of NTs on nuclear and cytosolic signals have been recognized as favoring increased synaptic transmission and plasticity, cell proliferation, and surviva...

show abstract

mentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Cigarette Smoke–Induced Airway Hyperreactivity

Sathish¹,

VanOosten²,

Miller³

et al. 2013

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…The occurrence of Ross syndrome in identical twins suggests that genetics may have a role in the pathogenesis of the disease, possibly through the involvement of multiple genes affecting the development or the survival of selective populations of sympathetic neurons. 7 We cannot exclude an interaction between genetic and environmental factors which may have exerted their effect during early childhood or intrauterine life, although the clinical history of the 2 brothers during these life stages was unremarkable.…”

mentioning

confidence: 95%

Ross syndrome

Nolano

Provitera

Donadio³

et al. 2013

Neurology

View full text Add to dashboard Cite

“…For example, the sigma-1 receptor causes the pathway for neuroactive ligand-receptor interaction to malfunction, leading to memory process and cognitive disorders [42]. Sympathetic changes lead to disorders in the neurotrophin signalling pathway [44]. Similarly and equally importantly, the Fc epsilon RI signalling pathway can be detected in injured cardiac mast cells [48].…”

Section: Analysis Results From Two Prostate Tumour Microarray Datasetsmentioning

confidence: 99%

A novel method to quantify gene set functional association based on gene ontology

Wang

et al. 2011

J. R. Soc. Interface.

View full text Add to dashboard Cite

Numerous gene sets have been used as molecular signatures for exploring the genetic basis of complex disorders. These gene sets are distinct but related to each other in many cases; therefore, efforts have been made to compare gene sets for studies such as those evaluating the reproducibility of different experiments. Comparison in terms of biological function has been demonstrated to be helpful to biologists. We improved the measurement of semantic similarity to quantify the functional association between gene sets in the context of gene ontology and developed a web toolkit named Gene Set Functional Similarity (GSFS; http://bioinfo.hrbmu.edu.cn/GSFS). Validation based on protein complexes for which the functional associations are known demonstrated that the GSFS scores tend to be correlated with sequence similarity scores and that complexes with high GSFS scores tend to be involved in the same functional catalogue. Compared with the pairwise method and the annotation method, the GSFS shows better discrimination and more accurately reflects the known functional catalogues shared between complexes. Case studies comparing differentially expressed genes of prostate tumour samples from different microarray platforms and identifying coronary heart disease susceptibility pathways revealed that the method could contribute to future studies exploring the molecular basis of complex disorders.

show abstract

Neurotrophins and target interactions in the development and regulation of sympathetic neuron electrical and synaptic properties

Cited by 41 publications

References 210 publications

Brain-Derived Neurotrophic Factor in Cigarette Smoke–Induced Airway Hyperreactivity

Brain-Derived Neurotrophic Factor in Cigarette Smoke–Induced Airway Hyperreactivity

Ross syndrome

A novel method to quantify gene set functional association based on gene ontology

Contact Info

Product

Resources

About