Articles producció científica> Ciències Mèdiques Bàsiques

TrkB signaling is correlated with muscular fatigue resistance and less vulnerability to neurodegeneration

  • Identification data

    Identifier: imarina:9287836
    Authors:
    Just-Borras, LaiaCilleros-Mane, VictorPolishchuk, AleksandraBalanya-Segura, MartaTomas, MartaGarcia, NeusTomas, JosepLanuza, Maria A
    Abstract:
    At the neuromuscular junction (NMJ), motor neurons and myocytes maintain a bidirectional communication that guarantees adequate functionality. Thus, motor neurons’ firing pattern, which is influenced by retrograde muscle-derived neurotrophic factors, modulates myocyte contractibility. Myocytes can be fast-twitch fibers and become easily fatigued or slow-twitch fibers and resistant to fatigue. Extraocular muscles (EOM) show mixed properties that guarantee fast contraction speed and resistance to fatigue and the degeneration caused by Amyotrophic lateral sclerosis (ALS) disease. The TrkB signaling is an activity-dependent pathway implicated in the NMJ well-functioning. Therefore, it could mediate the differences between fast and slow myocytes’ resistance to fatigue. The present study elucidates a specific protein expression profile concerning the TrkB signaling that correlates with higher resistance to fatigue and better neuroprotective capacity through time. The results unveil that Extra-ocular muscles (EOM) express lower levels of NT-4 that extend TrkB signaling, differential PKC expression, and a higher abundance of phosphorylated synaptic proteins that correlate with continuous neurotransmission requirements. Furthermore, common molecular features between EOM and slow soleus muscles including higher neurotrophic consumption and classic and novel PKC isoforms balance correlate with better preservation of these two muscles in ALS. Altogether, higher resistance of Soleus and EOM to fatigue and ALS seems to be associated with specific protein levels concerning the TrkB neurotrophic signaling.
  • Others:

    Author, as appears in the article.: Just-Borras, Laia; Cilleros-Mane, Victor; Polishchuk, Aleksandra; Balanya-Segura, Marta; Tomas, Marta; Garcia, Neus; Tomas, Josep; Lanuza, Maria A
    Department: Ciències Mèdiques Bàsiques
    URV's Author/s: Balanya Segura, Marta / Cilleros Mañé, Víctor / Garcia Sancho, Maria de les Neus / Just Borràs, Laia / Lanuza Escolano, María Angel / POLISHCHUK, ALEKSANDRA / Tomás Ferré, José Maria / Tomas Marginet, Marta
    Keywords: Trkb-bdnf Skeletal muscle Protein-kinase-c Pkc Pka Neuromuscular junction Fatigue-resistant Eom synaptosome-associated protein skeletal-muscle skeletal muscle pkc pka neurotrophic factor neurotransmitter release neuromuscular-transmission neuromuscular junction motor-neuron fiber-type fatigue-resistant eom differential phosphorylation dependent phosphorylation
    Abstract: At the neuromuscular junction (NMJ), motor neurons and myocytes maintain a bidirectional communication that guarantees adequate functionality. Thus, motor neurons’ firing pattern, which is influenced by retrograde muscle-derived neurotrophic factors, modulates myocyte contractibility. Myocytes can be fast-twitch fibers and become easily fatigued or slow-twitch fibers and resistant to fatigue. Extraocular muscles (EOM) show mixed properties that guarantee fast contraction speed and resistance to fatigue and the degeneration caused by Amyotrophic lateral sclerosis (ALS) disease. The TrkB signaling is an activity-dependent pathway implicated in the NMJ well-functioning. Therefore, it could mediate the differences between fast and slow myocytes’ resistance to fatigue. The present study elucidates a specific protein expression profile concerning the TrkB signaling that correlates with higher resistance to fatigue and better neuroprotective capacity through time. The results unveil that Extra-ocular muscles (EOM) express lower levels of NT-4 that extend TrkB signaling, differential PKC expression, and a higher abundance of phosphorylated synaptic proteins that correlate with continuous neurotransmission requirements. Furthermore, common molecular features between EOM and slow soleus muscles including higher neurotrophic consumption and classic and novel PKC isoforms balance correlate with better preservation of these two muscles in ALS. Altogether, higher resistance of Soleus and EOM to fatigue and ALS seems to be associated with specific protein levels concerning the TrkB neurotrophic signaling.
    Thematic Areas: Neurosciences Molecular biology Medicina ii Ciências biológicas ii Cellular and molecular neuroscience
    licence for use: https://creativecommons.org/licenses/by/3.0/es/
    Author's mail: marta.balanya@urv.cat aleksandra.polishchuk@urv.cat laia.just@urv.cat marta.tomas@urv.cat aleksandra.polishchuk@urv.cat marta.balanya@urv.cat victor.cilleros@alumni.urv.cat josepmaria.tomas@urv.cat laia.just@urv.cat mariaangel.lanuza@urv.cat
    Author identifier: 0000-0003-0983-4944 0000-0001-6445-1538 0000-0003-0473-3730 0000-0002-4151-1697 0000-0001-6445-1538 0000-0003-0983-4944 0000-0001-5690-9932 0000-0002-0406-0006 0000-0003-0473-3730 0000-0003-4795-4103
    Record's date: 2024-10-12
    Papper version: info:eu-repo/semantics/publishedVersion
    Link to the original source: https://www.frontiersin.org/articles/10.3389/fnmol.2022.1069940/full
    Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
    Papper original source: Frontiers In Molecular Neuroscience. 15 1069940-
    APA: Just-Borras, Laia; Cilleros-Mane, Victor; Polishchuk, Aleksandra; Balanya-Segura, Marta; Tomas, Marta; Garcia, Neus; Tomas, Josep; Lanuza, Maria A (2022). TrkB signaling is correlated with muscular fatigue resistance and less vulnerability to neurodegeneration. Frontiers In Molecular Neuroscience, 15(), 1069940-. DOI: 10.3389/fnmol.2022.1069940
    Article's DOI: 10.3389/fnmol.2022.1069940
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2022
    Publication Type: Journal Publications
  • Keywords:

    Cellular and Molecular Neuroscience,Molecular Biology,Neurosciences
    Trkb-bdnf
    Skeletal muscle
    Protein-kinase-c
    Pkc
    Pka
    Neuromuscular junction
    Fatigue-resistant
    Eom
    synaptosome-associated protein
    skeletal-muscle
    skeletal muscle
    pkc
    pka
    neurotrophic factor
    neurotransmitter release
    neuromuscular-transmission
    neuromuscular junction
    motor-neuron
    fiber-type
    fatigue-resistant
    eom
    differential phosphorylation
    dependent phosphorylation
    Neurosciences
    Molecular biology
    Medicina ii
    Ciências biológicas ii
    Cellular and molecular neuroscience
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