miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.
Animals
Cell Differentiation
Cell Proliferation
Collagen
/ metabolism
Disease Progression
Dystrophin
/ deficiency
Female
Humans
Male
Mice
Mice, Inbred C57BL
Mice, Inbred mdx
Mice, Knockout
MicroRNAs
/ genetics
Muscle, Skeletal
/ metabolism
Muscular Dystrophy, Animal
/ genetics
Muscular Dystrophy, Duchenne
/ genetics
RNA, Messenger
/ genetics
Satellite Cells, Skeletal Muscle
/ metabolism
Transforming Growth Factor beta1
/ genetics
Up-Regulation
Duchenne muscular dystrophy
Inflammation
Regeneration
Skeletal muscle
mdx
miR-146a
Journal
Skeletal muscle
ISSN: 2044-5040
Titre abrégé: Skelet Muscle
Pays: England
ID NLM: 101561193
Informations de publication
Date de publication:
14 08 2019
14 08 2019
Historique:
received:
20
02
2019
accepted:
31
07
2019
entrez:
16
8
2019
pubmed:
16
8
2019
medline:
6
5
2020
Statut:
epublish
Résumé
Duchenne muscular dystrophy (DMD) is a genetic disease evoked by a mutation in the dystrophin gene. It is associated with progressive muscle degeneration and increased inflammation. Up to this date, mainly anti-inflammatory treatment is available for patients suffering from DMD. miR-146a is known to diminish inflammation and fibrosis in different tissues by downregulating the expression of proinflammatory cytokines. However, its role in DMD has not been studied so far.In our work, we have generated mice globally lacking both dystrophin and miR-146a (miR-146a
Identifiants
pubmed: 31412923
doi: 10.1186/s13395-019-0207-0
pii: 10.1186/s13395-019-0207-0
pmc: PMC6693262
doi:
Substances chimiques
Dystrophin
0
MicroRNAs
0
Mirn146 microRNA, mouse
0
RNA, Messenger
0
Tgfb1 protein, mouse
0
Transforming Growth Factor beta1
0
Collagen
9007-34-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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