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FM19G11-loaded nanoparticles modulate energetic status and production of reactive oxygen species in myoblasts from ALS mice

Fecha de publicación: Fecha Ahead of Print:

Autores de CIPF

Participantes ajenos a CIPF

  • Malacarne, C
  • Giagnorio, E
  • Chirizzi, C
  • Cattaneo, M
  • Saraceno, F
  • Cavalcante, P
  • Bonanno, S
  • Mantegazza, R
  • Lauria, G
  • Metrangolo, P
  • Bombelli, FB
  • Marcuzzo, S

Grupos de Investigación

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. Considerable evidence indicates that early skeletal muscle atrophy plays a crucial role in the disease pathogenesis, leading to an altered muscle-motor neuron crosstalk that, in turn, may contribute to motor neuron degeneration. Currently, there is no effective treatment for ALS, highlighting the need to dig deeper into the pathological mechanisms for developing innovative therapeutic strategies. FM19G11 is a novel drug able to modulate the global cellular metabolism, but its effects on ALS skeletal muscle atrophy and mitochondrial metabolism have never been evaluated, yet. This study investigated whether FM19G11-loaded nanoparticles (NPs) may affect the bioenergetic status in myoblasts isolated from G93A-SOD1 mice at different disease stages. We found that FM19G1-loaded NP treatment was able to increase transcriptional levels of Akt1, Akt3, Mef2a, Mef2c and Ucp2, which are key genes associated with cell proliferation (Akt1, Akt3), muscle differentiation (Mef2c), and mitochondrial activity (Ucp2), in G93A-SOD1 myoblasts. These cells also showed a significant reduction of mitochondrial area and networks, in addition to decreased ROS production after treatment with FM19G11-loaded NPs, suggesting a ROS clearance upon the amelioration of mitochondrial dynamics. Our overall findings demonstrate a significant impact of FM19G11-loaded NPs on muscle cell function and bioenergetic status in G93A-SOD1 myoblasts, thus promising to open new avenues towards possible adoption of FM19G11-based nanotherapies to slow muscle degeneration in the frame of ALS and muscle disorders.

Datos de la publicación

ISSN/ISSNe:
0753-3322, 1950-6007

BIOMEDICINE & PHARMACOTHERAPY  Elsevier Masson

Tipo:
Article
Páginas:
-
PubMed:
38447450

Citas Recibidas en Web of Science: 1

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Keywords

  • Amyotrophic lateral sclerosis; Muscle; G93A-SOD1 mouse model; Nanomedicine

Campos de Estudio

Financiación

CALabria HUB per Ricerca Innovativa ed Avanzata- CALHUB.RIA "Creazione di Hub delle Scienze della Vita" T4 -AN -09 prog. ZRPOS2
Fondazione Regionale per la Ricerca Biomedica POR FESR 2014-2020 under INTERSLA project (1157625)
Italian Ministry of Health

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COMMISSION OF EUROPEAN COMMUNITIES . 2021

ESTRATEGIAS DE TERAPIA CELULAR PARA LA REGENERACIÓN DE LESIONES MEDULARES

Investigador Principal: M VICTORIA MORENO MANZANO

MINISTERIO DE CIENCIA, INNOVACION Y UNIVERSIDADES . 2022

Modelos de transcriptomica espacial y comunicación celular aplicados a la regeneracion tisular y tratamiento en daño de espina dorsal. Coordina Ana Conesa del CSIC, colaboran MJ.Vicent, V.Moreno, A.Alastrue y A.Armiñan del CIPF

CONSELLERIA DE EDUCACION . 2023

MULTISMART, Multi-component Soft Materials Advanced Research Training Network

Investigador Principal: MARIA JESUS VICENT DOCON

COMMISSION OF EUROPEAN COMMUNITIES . 2023

Predoc Samuel

Investigador Principal: M VICTORIA MORENO MANZANO

MINISTERIO DE CIENCIA, INNOVACION Y UNIVERSIDADES . 2023

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