The physiology of regulated BDNF release

Brigadski, Tanja; Leßmann, Volkmar

doi:10.1007/s00441-020-03253-2

Cited by 102 publications

(88 citation statements)

References 241 publications

(358 reference statements)

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“…BDNF expression and TrkB signaling, as well as their significance in the normal physiological and pathophysiological processes in the lungs continue to be explored [ 17 ]. Specifically, various stimuli affecting intra- and extracellular BDNF concentration have been analyzed with a view to understand the relevance of major variations of BDNF levels in human blood and tissue [ 19 ]. A number of studies thus far have sought to investigate the role of BDNF in the airways by assessing its concentration locally and in the peripheral circulation, as well as by determining the association between selected polymorphisms in the BDNF and NTRK2 ( TrkB ) genes and the development of asthma [ 9 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Plasma Brain-Derived Neurotrophic Factor (BDNF) Concentration and BDNF/TrkB Gene Polymorphisms in Croatian Adults with Asthma

Sreter¹,

Popović‐Grle

Lampalo

et al. 2020

JPM

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Brain-derived neurotrophic factor (BDNF) and its tropomyosin-related kinase B (TrkB) receptor might contribute to normal lung functioning and immune responses; however, their role in asthma remains unclear. Plasma BDNF concentration, as well as BDNF and NTRK2 (TrkB gene) polymorphisms, were investigated in 120 asthma patients and 120 healthy individuals using enzyme-linked immunosorbent assay and polymerase chain reaction, respectively. The genotype and allele frequencies of BDNF Val66Met (rs6265) and NTRK2 rs1439050 polymorphisms did not differ between healthy individuals and asthma patients, nor between patients grouped according to severity or different asthma phenotypes. Although plasma BDNF concentrations were higher among healthy subjects carrying the BDNF Val66Met GG genotype compared to the A allele carriers, such differences were not detected in asthma patients, suggesting the influences of other factors. Plasma BDNF concentration was not affected by NTRK2 rs1439050 polymorphism. Asthma patients had higher plasma BDNF concentrations than control subjects; however, no differences were found between patients subdivided according to asthma severity, or Type-2, allergic, and eosinophilic asthma. Higher plasma BDNF levels were observed in asthma patients with aspirin sensitivity and aspirin-exacerbated respiratory disease. These results suggest that plasma BDNF may serve as a potential peripheral biomarker for asthma, particularly asthma with aspirin sensitivity.

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Section: Introductionmentioning

confidence: 99%

Plasma Brain-Derived Neurotrophic Factor (BDNF) Concentration and BDNF/TrkB Gene Polymorphisms in Croatian Adults with Asthma

Sreter¹,

Popović‐Grle

Lampalo

et al. 2020

JPM

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“…It is well accepted that muscle contraction-induced myokine release, particularly BDNF, has neurotrophic and neuroprotective effects [ 68 ]. The neurotrophic factor BDNF is an important regulator for the development of brain circuits, neuronal development, synaptic and neuronal network plasticity, as well as for neuroregeneration and neuroprotection and modulation of synaptic activity [ 69 ]. Independently of the neuronal properties, neurotrophins exert unique cardiovascular activities.…”

Section: Modulatory Role Of Myokines On Ros In the Context Of I/rmentioning

confidence: 99%

Modulatory Effect of Myokines on Reactive Oxygen Species in Ischemia/Reperfusion

Szabó

Pipicz

Csont

et al. 2020

IJMS

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There is a growing body of evidence showing the importance of physical activity against acute ischemic events in various organs. Ischemia/reperfusion injury (I/R) is characterized by tissue damage as a result of restriction and subsequent restoration of blood supply to an organ. Oxidative stress due to increased reactive oxygen species formation and/or insufficient antioxidant defense is considered to play an important role in I/R. Physical activity not only decreases the general risk factors for ischemia but also confers direct anti-ischemic protection via myokine production. Myokines are skeletal muscle-derived cytokines, representing multifunctional communication channels between the contracting skeletal muscle and other organs through an endocrine manner. In this review, we discuss the most prominent members of the myokines (i.e., brain-derived neurotrophic factor (BDNF), cathepsin B, decorin, fibroblast growth factors-2 and -21, follistatin, follistatin-like, insulin-like growth factor-1; interleukin-6, interleukin-7, interleukin-15, irisin, leukemia inhibitory factor, meteorin-like, myonectin, musclin, myostatin, and osteoglycin) with a particular interest in their potential influence on reactive oxygen and nitrogen species formation or antioxidant capacity. A better understanding of the mechanism of action of myokines and particularly their participation in the regulation of oxidative stress may widen their possible therapeutic use and, thereby, may support the fight against I/R.

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“…Brain-derived neurotrophic factor (BDNF) is synthesized as a precursor (proBDNF) in the endoplasmic reticulum that can be proteolytically cleaved and thereby converted into mature BDNF (mBDNF) 1 – 3 . Cleavage of proBDNF can take place either intracellularly in the Golgi or in secretory vesicles by furin or proprotein convertases 4 or through extracellular action of matrix metalloproteinases or components of the tissue plasminogen activator/plasmin (tPA/plasmin) proteolytic cascade 5 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Long-term depression at hippocampal mossy fiber-CA3 synapses involves BDNF but is not mediated by p75NTR signaling

Garad

Edelmann

Leßmann

2021

Sci Rep

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BDNF plays a crucial role in the regulation of synaptic plasticity. It is synthesized as a precursor (proBDNF) that can be proteolytically cleaved to mature BDNF (mBDNF). Previous studies revealed a bidirectional mode of BDNF actions, where long-term potentiation (LTP) was mediated by mBDNF through tropomyosin related kinase (Trk) B receptors whereas long-term depression (LTD) depended on proBDNF/p75 neurotrophin receptor (p75NTR) signaling. While most experimental evidence for this BDNF dependence of synaptic plasticity in the hippocampus was derived from Schaffer collateral (SC)-CA1 synapses, much less is known about the mechanisms of synaptic plasticity, in particular LTD, at hippocampal mossy fiber (MF) synapses onto CA3 neurons. Since proBDNF and mBDNF are expressed most abundantly at MF-CA3 synapses in the rodent brain and we had shown previously that MF-LTP depends on mBDNF/TrkB signaling, we now explored the role of proBDNF/p75NTR signaling in MF-LTD. Our results show that neither acute nor chronic inhibition of p75NTR signaling impairs MF-LTD, while short-term plasticity, in particular paired-pulse facilitation, at MF-CA3 synapses is affected by a lack of functional p75NTR signaling. Furthermore, MF-CA3 synapses showed normal LTD upon acute inhibition of TrkB receptor signaling. Nonetheless, acute inhibition of plasminogen activator inhibitor-1 (PAI-1), an inhibitor of both intracellular and extracellular proBDNF cleavage, impaired MF-LTD. This seems to indicate that LTD at MF-CA3 synapses involves BDNF, however, MF-LTD does not depend on p75NTRs. Altogether, our experiments demonstrate that p75NTR signaling is not warranted for all glutamatergic synapses but rather needs to be checked separately for every synaptic connection.

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The physiology of regulated BDNF release

Cited by 102 publications

References 241 publications

Plasma Brain-Derived Neurotrophic Factor (BDNF) Concentration and BDNF/TrkB Gene Polymorphisms in Croatian Adults with Asthma

Plasma Brain-Derived Neurotrophic Factor (BDNF) Concentration and BDNF/TrkB Gene Polymorphisms in Croatian Adults with Asthma

Modulatory Effect of Myokines on Reactive Oxygen Species in Ischemia/Reperfusion

Long-term depression at hippocampal mossy fiber-CA3 synapses involves BDNF but is not mediated by p75NTR signaling

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