Endothelial cells are an important source of BDNF in rat skeletal muscle.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
10 01 2022
10 01 2022
Historique:
received:
16
07
2021
accepted:
09
12
2021
entrez:
11
1
2022
pubmed:
12
1
2022
medline:
22
2
2022
Statut:
epublish
Résumé
BDNF (brain-derived neurotrophic factor) is present in skeletal muscle, controlling muscular metabolism, strength and regeneration processes. However, there is no consensus on BDNF cellular source. Furthermore, while endothelial tissue expresses BDNF in large amount, whether endothelial cells inside muscle expressed BDNF has never been explored. The aim of the present study was to provide a comprehensive analysis of BDNF localization in rat skeletal muscle. Cellular localization of BDNF and activated Tropomyosin-related kinase B (TrkB) receptors was studied by immunohistochemical analysis on soleus (SOL) and gastrocnemius (GAS). BDNF and activated TrkB levels were also measured in muscle homogenates using Western blot analysis and/or Elisa tests. The results revealed BDNF immunostaining in all cell types examined with a prominent staining in endothelial cells and a stronger staining in type II than type I muscular fibers. Endothelial cells but not other cells displayed easily detectable activated TrkB receptor expression. Levels of BDNF and activated TrkB receptors were higher in SOL than GAS. In conclusion, endothelial cells are an important and still unexplored source of BDNF present in skeletal muscle. Endothelial BDNF expression likely explains why oxidative muscle exhibits higher BDNF levels than glycolytic muscle despite higher the BDNF expression by type II fibers.
Identifiants
pubmed: 35013359
doi: 10.1038/s41598-021-03740-8
pii: 10.1038/s41598-021-03740-8
pmc: PMC8748777
doi:
Substances chimiques
Bdnf protein, rat
0
Brain-Derived Neurotrophic Factor
0
Ntrk2 protein, rat
EC 2.7.10.1
Receptor, trkB
EC 2.7.10.1
Types de publication
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
311Informations de copyright
© 2022. The Author(s).
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