The Role of BDNF in Peripheral Nerve Regeneration: Activity-Dependent Treatments and Val66Met

McGregor, Claire; English, Arthur W.

doi:10.3389/fncel.2018.00522

Cited by 123 publications

(105 citation statements)

References 293 publications

(379 reference statements)

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“…However, when NGF–TrkA complexes are not internalized, activation of the phosphatidylinositol 3‐kinase and Akt/protein kinase B (PI3K/Akt) pathways arise, which regulate cell survival and neurite extension (Gomez & Schmidt, 2007; Madduri et al, 2009; Tang et al, 2013). When BDNF binds to TrkB receptors, the PI3K/Akt pathway is triggered and microtubules are rearranged to encourage filopodial elongation and lamellipodial formation (Mcgregor & English, 2019). Hence, Trk receptors activate signaling pathways which encourage neurite elongation in sensory and motor neurons.…”

Section: Discussionmentioning

confidence: 99%

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Biomimetic surface delivery of NGF and BDNF to enhance neurite outgrowth

Sandoval-Castellanos

Claeyssens

Haycock

2020

Biotech & Bioengineering

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Treatment for peripheral nerve injuries includes the use of autografts and nerve guide conduits (NGCs). However, outcomes are limited, and full recovery is rarely achieved. The use of nerve scaffolds as a platform to surface immobilize neurotrophic factors and deliver locally is a promising approach to support neurite and nerve outgrowth after injury. We report on a bioactive surface using functional amine groups, to which heparin binds electrostatically. X‐ray photoelectron spectroscopy analysis was used to characterize the presence of nitrogen and sulfur. Nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF) were bound by electrostatic interaction to heparin, and the release profile evaluated by enzyme‐linked immunosorbent assay, which showed that ca. 1% of NGF was released from each of the bioactive surface within 7 days. Furthermore, each surface showed a maximum release of 97% of BDNF. Neurotrophin release on neurite outgrowth was evaluated by primary dorsal root ganglion with a maximum neurite growth response in vitro of 1,075 µm detected for surfaces immobilized with NGF at 1 ng/ml. In summary, the study reports on the design and construction of a biomimetic platform to deliver NGF and BDNF using physiologically low concentrations of neurotrophin. The platform is directly applicable and scalable for improving the regenerative ability of existing NGCs and scaffolds.

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Section: Discussionmentioning

confidence: 99%

“…Self‐regeneration may occur if the injury is not severe. However, as the degree of injury increases, recovery of sensory and motor function is often incomplete (Hu, Tian, Prabhakaran, Ding, & Ramakrishna, 2016; Mcgregor & English, 2019). Autografting is a standard clinical approach to treat regeneration of completely transected nerves.…”

Section: Introductionmentioning

confidence: 99%

Biomimetic surface delivery of NGF and BDNF to enhance neurite outgrowth

Sandoval-Castellanos

Claeyssens

Haycock

2020

Biotech & Bioengineering

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“…BDNF, a member of neurotrophin family, is the most studied neurotrophic factor due to its abundance in nervous system and brain. BDNF plays important roles in development, differentiation, maintenance, and regeneration of neurons (75,76). It signals through p75 neurotrophin receptor and tropomyosin receptor kinases (77), which are expressed primarily in neurons as well as in a variety of tissues including the liver, pancreas, colon, breast, immune system, muscles, and prostrate.…”

Section: Brain-derived Neurotrophic Factormentioning

confidence: 99%

Hepatic Autonomic Nervous System and Neurotrophic Factors Regulate the Pathogenesis and Progression of Non-alcoholic Fatty Liver Disease

Amir

et al. 2020

Front. Med.

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Non-alcoholic fatty liver disease represents a continuum of excessive hepatic steatosis, inflammation and fibrosis. It is a growing epidemic in the United States of America and worldwide. Progression of non-alcoholic fatty liver disease can lead to morbidity and mortality due to complications such as cirrhosis or hepatocellular carcinoma. Pathogenesis of non-alcoholic fatty liver disease is centered on increased hepatic lipogenesis and decreased hepatic lipolysis in the setting of hepatic and systemic insulin resistance. Adipose tissue and hepatic inflammation can further perpetuate the severity of illness. Currently there are no approved therapies for non-alcoholic fatty liver disease. Most of the drugs being explored for non-alcoholic fatty liver disease focus on classical pathogenic pathways surrounding hepatic lipid accumulation, inflammation or fibrosis. Studies have demonstrated that the autonomic nervous system innervating the liver plays a crucial role in regulation of hepatic lipid homeostasis, inflammation and fibrosis. Additionally, there is growing evidence that neurotrophic factors can modulate all stages of non-alcoholic fatty liver disease. Both the autonomic nervous system and neurotrophic factors are altered in patients and murine models of non-alcoholic fatty liver disease. In this review we focus on the pathophysiological role of the autonomic nervous system and neurotrophic factors that could be potential targets for novel therapeutic approaches to treat non-alcoholic fatty liver disease.

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“…Cao, et al have recently suggested that sympathetic nerve plastically is dependent on cold-induced, adipose-derived NGF (63). Although they provide evidence that NGF is involved to some degree in promoting cold induced sympathetic nerve density and browning of scWAT, the cellular source of NGF was ambiguous (our data indicate it is produced more by mature adipocytes than SVF cells, and thus may be promoting innervation of the adipocytes and not the SVF (64). Following peripheral nerve injury local sources of secreted BDNF include not only dorsal root ganglia neurons but support cells, including Schwann cells (64).…”

Section: Discussionmentioning

confidence: 58%

The Involvement of Neuroimmune Cells in Adipose Innervation

Blaszkiewicz

Wood

Koizar

et al. 2020

Preprint

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Background: Innervation of adipose tissue is essential for the proper function of this critical metabolic organ. Numerous surgical and chemical denervation studies have demonstrated how maintenance of brain-adipose communication through both sympathetic efferent and sensory afferent nerves helps regulate adipocyte size, cell number, lipolysis, and ‘browning’ of white adipose tissue. Neurotrophic factors are growth factors that promote neuron survival, regeneration and plasticity, including neurite outgrowth and synapse formation. Peripheral blood immune cells have been shown to be a source of neurotrophic factors in humans and mice. Although a number of immune cells reside in the adipose stromal vascular fraction (SVF), it has remained unclear what roles they play in adipose innervation. We previously demonstrated that adipose immune cells secrete brain derived neurotrophic factor (BDNF). Methods: We now show that deletion of this neurotrophic factor from the myeloid lineage led to a ‘genetic denervation’ of inguinal subcutaneous white adipose tissue (scWAT), thereby causing decreased energy expenditure, increased adipose mass, and a blunted UCP1 response to cold stimulation. Results: We and others have previously shown that noradrenergic stimulation via cold exposure increases adipose innervation in the inguinal depot. Here we have identified a subset of myeloid cells that home to scWAT upon cold exposure and are Ly6C + CCR2 + Cx3CR1 + monocytes/macrophages that express noradrenergic receptors and BDNF. Conclusions: We propose that these cold induced neuroimmune cells (CINCs) are key players in maintaining adipose innervation as well as promoting adipose nerve remodeling under noradrenergic stimulation, such as cold exposure.

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The Role of BDNF in Peripheral Nerve Regeneration: Activity-Dependent Treatments and Val66Met

Cited by 123 publications

References 293 publications

Biomimetic surface delivery of NGF and BDNF to enhance neurite outgrowth

Biomimetic surface delivery of NGF and BDNF to enhance neurite outgrowth

Hepatic Autonomic Nervous System and Neurotrophic Factors Regulate the Pathogenesis and Progression of Non-alcoholic Fatty Liver Disease

The Involvement of Neuroimmune Cells in Adipose Innervation

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