Neurotrophic receptors in HSCs

2014 ◽  
Vol 15 (12) ◽  
pp. 1103-1103
Author(s):  
Laurie A Dempsey
Keyword(s):  
Neurotrophic Receptors

scholarly journals Structural Basis of SNT PTB Domain Interactions with Distinct Neurotrophic Receptors

2000 ◽  
Vol 6 (4) ◽  
pp. 921-929 ◽  
Author(s):  
Christophe Dhalluin ◽  
Kelley S Yan ◽  
Olga Plotnikova ◽  
Kyung W Lee ◽  
Lei Zeng ◽  
...  
Keyword(s):  
Structural Basis ◽  
Domain Interactions ◽  
Neurotrophic Receptors ◽  
Ptb Domain

Origin and evolution of the Trk family of neurotrophic receptors

2006 ◽  
Vol 31 (2) ◽  
pp. 179-192 ◽  
Author(s):  
Èlia Benito-Gutiérrez ◽  
Jordi Garcia-Fernàndez ◽  
Joan X. Comella
Keyword(s):  
Origin And Evolution ◽  
Neurotrophic Receptors

scholarly journals Parasite-Derived Neurotrophic Factor/trans-Sialidase of Trypanosoma cruzi Links Neurotrophic Signaling to Cardiac Innate Immune Response

2014 ◽  
Vol 82 (9) ◽  
pp. 3687-3696 ◽  
Author(s):  
Ryan Salvador ◽  
Daniel Aridgides ◽  
Mercio PereiraPerrin
Keyword(s):  
Innate Immunity ◽  
Trypanosoma Cruzi ◽  
Neurotrophic Factor ◽  
Neutralizing Antibodies ◽  
Tissue Growth ◽  
Content Type ◽  
Monocyte Chemoattractant Protein 1 ◽  
Neurotrophic Signaling ◽  
Neurotrophic Receptors ◽  
Dose Dependent Increase

ABSTRACTThe Chagas' disease parasiteTrypanosoma cruzielicits a potent inflammatory response in acutely infected hearts that keeps parasitism in check and triggers cardiac abnormalities. A most-studied mechanism underlying innate immunity inT. cruziinfection is Toll-like receptor (TLR) activation by lipids and other parasite molecules. However, yet-to-be-identified pathways should exist. Here, we show thatT. cruzistrongly upregulates monocyte chemoattractant protein 1 (MCP-1)/CCL2 and fractalkine (FKN)/CX3CL1 in cellular and mouse models of heart infection. Mechanistically, upregulation of MCP-1 and FKN stems from the interaction of parasite-derived neurotrophic factor (PDNF)/trans-sialidase with neurotrophic receptors TrkA and TrkC, as assessed by pharmacological inhibition, neutralizing antibodies, and gene silencing studies. Administration of a single dose of intravenous PDNF to naive mice results in a dose-dependent increase in MCP-1 and FKN in the heart and liver with pulse-like kinetics that peak at 3 h postinjection. Intravenous PDNF also augments MCP-1 and FKN in TLR signaling-deficient MyD88-knockout mice, underscoring the MyD88-independent action of PDNF. Although single PDNF injections do not increase MCP-1 and FKN receptors, multiple PDNF injections at short intervals up the levels of receptor transcripts in the heart and liver, suggesting that sustained PDNF triggers cell recruitment at infection sites. Thus, given that MCP-1 and FKN are chemokines essential to the recruitment of immune cells to combat inflammation triggers and to enhance tissue repair, our findings uncover a new mechanism in innate immunity againstT. cruziinfection mediated by Trk signaling akin to an endogenous inflammatory and fibrotic pathway resulting from cardiomyocyte-TrkA recognition by matricellular connective tissue growth factor (CTGF/CCN2).

scholarly journals Impact of neurotrophic factors combination therapy on retinitis pigmentosa

2020 ◽  
Vol 48 (11) ◽  
pp. 030006052096783
Author(s):  
Xiaobei Yin ◽  
Ting He ◽  
Rui Chen ◽  
Hui Cui ◽  
Genlin Li
Keyword(s):  
Neurotrophic Factors ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Receptor Kinase ◽  
Dynamic Changes ◽  
Combined Use ◽  
Mrna And Protein Expression ◽  
Neurotrophic Receptors ◽  
Trk B ◽  
Ciliary Neurotrophic Factor Receptor

Objective We aimed to determine the location of neurotrophic receptors tropomyosin receptor kinase (Trk)B, TrkC, and ciliary neurotrophic factor receptor (CNTFR)α in the retina of retinal degeneration ( rd) mice and to explore the dynamic changes of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X-protein (Bax), and microtubule-associated protein light chain 3 (LC3) expression and ultrastructure in the retina of rd mice intravitreally injected with neurotrophic factors. Methods Rd mice aged 2 and 3 weeks post-natally (PN) received intravitreal injections of neurotrophic factors. Two weeks later, their retinas were harvested for the detection of Bax, Bcl-2, and LC3 mRNA and protein expression. Results TrkB and TrkC expression levels were lower at 3 weeks PN compared with 0, 1, and 2 weeks PN, but CNTFRα expression was still detected in certain layers. The three receptors were expressed in different retinal layers at the same timepoint. Bax expression was downregulated in, rhBDNF + rhCNTF, rhBDNF + rhNT-3, groups 2 weeks after intravitreal injection; Bcl-2 expression was upregulated in the rhBDNF + rhCNTF + rhNT-3 group at PN-4w; and LC3 expression was upregulated in rhBDNF + rhCNTF + rhNT-3 groups. Conclusions The combined use of neurotrophic factors had a more significant effect on Bax, Bcl-2, and LC3 expression than the same factors used alone.

scholarly journals Role of BDNF and neurotrophic receptors in human inner ear development

2017 ◽  
Vol 370 (3) ◽  
pp. 347-363 ◽  
Author(s):  
L. Johnson Chacko ◽  
M. J. F. Blumer ◽  
E. Pechriggl ◽  
H. Rask-Andersen ◽  
W. Dietl ◽  
...  
Keyword(s):  
Inner Ear ◽  
Ear Development ◽  
Inner Ear Development ◽  
Neurotrophic Receptors ◽  
Human Inner Ear

scholarly journals Matrix metalloproteinases, purinergic signaling, and epigenetics, hubs in the spinal neuroglial network following nerve injury.

2021 ◽  
Author(s):  
Ciro De Luca ◽  
Assunta Virtuoso ◽  
Nicola Maggio ◽  
Michele Cerasuolo ◽  
Anna Maria Colangelo ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Nerve Injury ◽  
Purinergic Signaling ◽  
Neurological Diseases ◽  
Network Failure ◽  
Targeted Treatments ◽  
Complex Protein ◽  
Spinal Network ◽  
Network Consistency ◽  
Neurotrophic Receptors

Abstract The neuroglial network characterizes synaptic transmission and accounts for both cellular elements (neurons and glia) and neural extracellular matrix (nECM) roles. Glial cells, neuron, and nECMnetwork is strongly interconnected, in physiological and pathological conditions as shownin several neurodegenerative diseases. Purinergic activation and matrix metalloproteinases (MMPs) remodeling of the spinal cord is pivotal in maladaptive plastic changes following peripheral nerve injury (PNI). To understand how purinergic and MMPs inhibition may modulate and potentially reverse the neuroglial network failure, we used the spared nerve injury (SNI) model of the sciatic nerve. Molecular and morphological analysis of astrocytic and microglial activation, purinergic and neurotrophic receptors, Histone Deacetylase (HDAC)1, HDAC2 were analyzed to define the pathways in response to the purinergic and MMPs inhibition. The data suggest complex protein interconnections, which are not passively influenced by epigenetics but actively contribute to modify the transcriptomics machinery. The present study contributes to unveiling the spinal network consistency and ultimately encourages new paths for targeted treatments in neurological diseases with benefits of neuroprotection, plasticity, and functional recovery.

Neurotrophic Receptors as Potential Therapy Targets in Postnatal Development, in Adult, and in Hearing Loss-Affected Inner Ear

2011 ◽  
Vol 32 (5) ◽  
pp. 761-773 ◽  
Author(s):  
Mario Bitsche ◽  
Jozsef Dudas ◽  
Soumen Roy ◽  
Thomas Potrusil ◽  
Joachim Schmutzhard ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inner Ear ◽  
Postnatal Development ◽  
Therapy Targets ◽  
Neurotrophic Receptors

trking neurotrophic receptors

Nature ◽  
1991 ◽  
Vol 350 (6320) ◽  
pp. 660-661 ◽  
Author(s):  
Cliff Ragsdale ◽  
Jim Woodgett
Keyword(s):  
Neurotrophic Receptors

scholarly journals FRS2 PTB Domain Conformation Regulates Interactions with Divergent Neurotrophic Receptors

2002 ◽  
Vol 277 (19) ◽  
pp. 17088-17094 ◽  
Author(s):  
Kelley S. Yan ◽  
Miklos Kuti ◽  
Sherry Yan ◽  
Shiraz Mujtaba ◽  
Amjad Farooq ◽  
...  
Keyword(s):  
Neurotrophic Receptors ◽  
Ptb Domain

scholarly journals Signaling adaptor ShcD suppresses extracellular signal-regulated kinase (Erk) phosphorylation distal to the Ret and Trk neurotrophic receptors

2017 ◽  
Vol 292 (14) ◽  
pp. 5748-5759 ◽  
Author(s):  
Melanie K. B. Wills ◽  
Ava Keyvani Chahi ◽  
Hayley R. Lau ◽  
Manali Tilak ◽  
Brianna D. Guild ◽  
...  
Keyword(s):  
Extracellular Signal Regulated Kinase ◽  
Erk Phosphorylation ◽  
Extracellular Signal ◽  
Neurotrophic Receptors
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