Myofiber Type Shift in Extraocular Muscles in Amyotrophic Lateral Sclerosis.
Journal
Investigative ophthalmology & visual science
ISSN: 1552-5783
Titre abrégé: Invest Ophthalmol Vis Sci
Pays: United States
ID NLM: 7703701
Informations de publication
Date de publication:
01 05 2023
01 05 2023
Historique:
medline:
22
5
2023
pubmed:
18
5
2023
entrez:
18
5
2023
Statut:
ppublish
Résumé
To investigate changes in myofiber composition in the global layer (GL) and orbital layer (OL) of extraocular muscles (EOMs) from terminal amyotrophic lateral sclerosis (ALS) donors. Medial recti muscles collected postmortem from spinal-onset ALS, bulbar-onset ALS, and healthy control donors were processed for immunofluorescence with antibodies against myosin heavy chain (MyHC) IIa, MyHCI, MyHCeom, laminin, neurofilaments, synaptophysin, acetylcholine receptor γ-subunit, and α-bungarotoxin. The proportion of myofibers containing MyHCIIa was significantly smaller and MyHCeom was significantly larger in the GL of spinal-onset ALS and bulbar-onset ALS donors compared to control donors. Changes in the GL were more prominent in the bulbar-onset ALS donors, with a significantly larger proportion of myofibers containing MyHCeom being present compared to spinal-onset ALS donors. There were no significant differences in the myofiber composition in the OL. In the spinal-onset ALS donors, the proportions of myofibers containing MyHCIIa in the GL and MyHCeom in the OL were significantly correlated with the disease duration. Neurofilament and synaptophysin were present at motor endplates of myofibers containing MyHCeom in ALS donors. The EOMs of terminal ALS donors displayed changes in the fast-type myofiber composition in the GL, with a more pronounced alteration in bulbar-onset ALS donors. Our results align with the worse prognosis and subclinical changes in eye movement function previously observed in bulbar-onset ALS patients and suggest that the myofibers in the OL might be more resistant to the pathological process in ALS.
Identifiants
pubmed: 37200039
pii: 2785628
doi: 10.1167/iovs.64.5.15
pmc: PMC10207955
doi:
Substances chimiques
Synaptophysin
0
Myosin Heavy Chains
EC 3.6.4.1
Protein Isoforms
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
15Références
Invest Ophthalmol Vis Sci. 2017 Jul 1;58(9):3708-3715
pubmed: 28738414
J Clin Neurol. 2018 Oct;14(4):464-471
pubmed: 30198218
Acta Neuropathol. 1992;84(4):372-7
pubmed: 1441918
APMIS. 1988 May;96(5):379-94
pubmed: 3288247
J Neurol. 2010 Jul;257(7):1134-40
pubmed: 20146069
Invest Ophthalmol Vis Sci. 2004 Dec;45(12):4233-9
pubmed: 15557425
Surg Neurol Int. 2015 Nov 16;6:171
pubmed: 26629397
PLoS One. 2013;8(2):e57473
pubmed: 23468993
Exp Cell Res. 2011 Apr 1;317(6):873-85
pubmed: 21277300
Sci Rep. 2021 Nov 11;11(1):22128
pubmed: 34764380
Surv Ophthalmol. 1995 May-Jun;39(6):451-84
pubmed: 7660301
Eur J Neurol. 2005 Dec;12(12):921-38
pubmed: 16324086
J Comp Neurol. 2005 Oct 31;491(4):352-66
pubmed: 16175553
Physiol Genomics. 2002;9(2):71-84
pubmed: 12006673
Invest Ophthalmol Vis Sci. 2010 Jul;51(7):3494-501
pubmed: 20181843
J Appl Physiol (1985). 2011 Oct;111(4):1178-89
pubmed: 21778415
Front Biosci (Schol Ed). 2012 Jun 01;4(4):1547-55
pubmed: 22652891
Acta Neuropathol. 2013 Jan;125(1):95-109
pubmed: 23143228
EBioMedicine. 2021 Dec;74:103732
pubmed: 34864363
J Neurol Sci. 1990 Nov;99(2-3):311-9
pubmed: 2086731
Lancet Neurol. 2018 May;17(5):423-433
pubmed: 29598923
Prog Brain Res. 2006;151:43-80
pubmed: 16221585
J Neural Transm Suppl. 1983;19:305-15
pubmed: 6583314
Invest Ophthalmol Vis Sci. 2018 Jan 1;59(1):539-548
pubmed: 29372252
Invest Ophthalmol Vis Sci. 2003 Apr;44(4):1419-25
pubmed: 12657575
Invest Ophthalmol Vis Sci. 2020 Dec 1;61(14):31
pubmed: 33369640
Med Genet. 2018;30(2):252-258
pubmed: 30220791
J Neurol Neurosurg Psychiatry. 2017 Jul;88(7):540-549
pubmed: 28057713
Amyotroph Lateral Scler. 2009 Oct-Dec;10(5-6):310-23
pubmed: 19922118
Nat Rev Neurol. 2014 Nov;10(11):661-70
pubmed: 25311585