Neurotrophins in murine viscera: a dynamic pattern from birth to adulthood

Lommatzsch, Marek; Quarcoo, David; Schulte‐Herbrüggen, Olaf; Weber, Heike; Virchow, J. Christian; Renz, Harald; Braun, Armin

doi:10.1016/j.ijdevneu.2005.05.009

Cited by 54 publications

(44 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite the name, BDNF is expressed in most tissues of the body at relatively high levels (25). BDNF in the blood could be derived from a number of these peripheral tissues, as well as from the brain.…”

Section: What Is Source Of the Serum Bdnf?mentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Sen

Duman

Sanacora

2008

Biological Psychiatry

1,094

715

View full text Add to dashboard Cite

show abstract

Section: What Is Source Of the Serum Bdnf?mentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Sen

Duman

Sanacora

2008

Biological Psychiatry

1,094

715

View full text Add to dashboard Cite

show abstract

“…The relevance of such effects lies in the recent recognition that circulating and local BDNF concentrations, as well as receptor expression, are increased in asthma (22,44). Furthermore, animal studies suggest a role for BDNF in airway inflammation, remodeling, and hyperreactivity (47,48).…”

Section: Neurotrophins and Asmmentioning

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

“…The BDNF, acting throughout TrkB, seems to participate in the inflammatory processes including the activation of macrophages . Interestingly, detectable levels of the two main TrkB ligands, the BDNF and NT-4/5 (Lommatzsch et al , 2005Nemoto et al 2000;Cassiman et al 2001) are also present in the liver, and did not change significantly during the postnatal live (Lommatzsch et al 2005), suggesting the possibility of paracrine and/or autocrine intrahepatic loops. Thus, it could be hypothesized that the persistence of erythroblastric islands in TrkB deficient animals might be due to an impaired ability of macrophages to remove and eliminate these structures due to their not being responsive to NTs.…”

Section: Discussionmentioning

confidence: 98%

“…Nevertheless, data about the expression of TrkB and its main ligands in this organ are scarce and unclear. Thus, RT-PCR on human and rat liver showed trace levels of TrkB (Yamamoto et al 1996;Nemoto et al 2000), BDNF, and NT-4/5 (Lommatzsch et al , 2005Nemoto et al 2000;Cassiman et al 2001). On the other hand, results from immunohistochemical studies are contradictory; whereas some authors (Shibayama and Koizumi 1996) were unable to detect any Trk in the human liver, others (Cassiman et al 2001) observed TrkB immunostaining in human and rat hepatic stellate cells (although RT-PCR failed to demonstrate mRNA transcripts for TrkB in freshly isolated rat hepatic stellate cells), in normal and pathological conditions (Cassiman et al 2002).…”

Section: Introductionmentioning

confidence: 95%

Expression of the neurotrophin receptor TrkB in the mouse liver

et al. 2006

View full text Add to dashboard Cite

Neurotrophins acting through Trk signal-transducing receptors play essential roles in the nervous system, and probably in some non-neuronal tissues. In the present study, we used RT-PCR, Western-blot and immunohistochemistry to investigate the occurrence and cellular localization of TrkB in the mouse liver, from newborns to 6 months. Furthermore, the structure of the liver in mice carrying a mutation in the trkB gene, resulting in a non-functional protein, was studied. The analysis of the DNA sequence showed that hepatic trkB gene is identical to the cerebral one, and TrkB mRNA and TrkB full-length protein (145 kDa) were detected at all the ages sampled. Immunohistochemistry revealed age-dependent changes in the pattern of TrkB expression. From 0 to 15 days, the TrkB was detected in morphologically and immunohistochemically identified monocyte-macrophage-dendric cells scattered throughout the organ, while in animals 3- and 6-months-old it was restricted to nerve fibres. Interestingly, there was a parallelism between TrkB expression by monocyte-macrophage-dendric cells and the presence of hepatic erythroblastic islands. In agreement with a possible role of TrkB on hepatic haematopoiesis, the liver of 15 days old TrkB (-/-) mice still contained erythroblastic islands, whereas they were absent in the wild-type littermates. Another striking finding was the absence of nerve profiles in the TrkB (-/-) animals. All together, present results support the role of TrkB in the murine liver in maintaining the innervation of the organ, and more importantly throughout an unknown mechanism in controlling the hepatic haematopoietic function.

show abstract

Neurotrophins in murine viscera: a dynamic pattern from birth to adulthood

Cited by 54 publications

References 48 publications

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

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

Expression of the neurotrophin receptor TrkB in the mouse liver

Contact Info

Product

Resources

About