Lateral rectus muscle differentiation potential in paralytic esotropia patients.
BMC Ophthalmol
; 21(1): 235, 2021 May 27.
Article
em En
| MEDLINE
| ID: mdl-34044792
PURPOSE AND BACKGROUND: Recently, we found that maximal medial rectus recession and lateral rectus resection in patients with complete lateral rectus paralysis resulted in a partial restoration of abduction. In an attempt to understand some of the mechanisms involved with this effect we examined gene expression profiles of lateral recti from these patients, with our focus being directed to genes related to myogenesis. MATERIALS AND METHODS: Lateral recti resected from patients with complete lateral rectus paralysis and those from concomitant esotropia (controls) were collected. Differences in gene expression profiles between these two groups were examined using microarray analysis and quantitative Reverse-transcription PCR (qRT-PCR). RESULTS: A total of 3056 differentially expressed genes (DEGs) were identified between these two groups. Within the paralytic esotropia group, 2081 genes were up-regulated and 975 down-regulated. The results of RT-PCR revealed that PAX7, MYOG, PITX1, SIX1 and SIX4 showed higher levels of expression, while that of MYOD a lower level of expression within the paralytic esotropia group as compared with that in the control group (p < 0.05). CONCLUSION: The decreased expression of MYOD in the paralytic esotropia group suggested that extraocular muscle satellite cell (EOMSCs) differentiation processes were inhibited. Whereas the high expression levels of PAX7, SIX1/4 and MYOG, suggested that the EOMSCs were showing an effective potential for differentiation. The stimulation resulting from muscle surgery may induce EOMSCs to differentiate and thus restore abduction function.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Esotropia
/
Doenças do Nervo Abducente
Tipo de estudo:
Observational_studies
Limite:
Humans
Idioma:
En
Revista:
BMC Ophthalmol
Assunto da revista:
OFTALMOLOGIA
Ano de publicação:
2021
Tipo de documento:
Article
País de afiliação:
China