Insulin-like growth factor-1 stimulates retinal cell proliferation via activation of multiple signaling pathways.
Cell proliferation
Central nervous system
Epidermal growth factor
Insulin-like growth factor-1
Retina
Signaling pathway
Journal
Current research in neurobiology
ISSN: 2665-945X
Titre abrégé: Curr Res Neurobiol
Pays: Netherlands
ID NLM: 101778135
Informations de publication
Date de publication:
2023
2023
Historique:
received:
17
07
2022
revised:
05
09
2022
accepted:
12
12
2022
entrez:
2
1
2023
pubmed:
3
1
2023
medline:
3
1
2023
Statut:
epublish
Résumé
Insulin-like growth factor-1 (IGF-1) plays critical roles in the development of the central nervous system (CNS), including the retina, regulating cell proliferation, differentiation, and survival. Here, we investigated the role of IGF-1 on retinal cell proliferation using primary cultures from rat neural retina. Our data show that IGF-1 stimulates retinal cell proliferation and regulates the expression of neurotrophic factors, such as interleukin-4 and brain-derived neurotrophic factor. In addition, our results indicates that IGF-1-induced retinal cell proliferation requires activation of multiple signaling pathways, including phosphatidylinositol 3-kinase, protein kinase Src, phospholipase-C, protein kinase C delta, and mitogen-activated protein kinase pathways. We further show that activation of matrix metalloproteinases and epidermal growth factor receptor is also necessary for IGF-1 enhancing retinal cell proliferation. Overall, these results unveil potential mechanisms by which IGF-1 ensures retinal cell proliferation and support the notion that manipulation of IGF-1 signaling may be beneficial in CNS disorders associated with abnormal cell proliferation.
Identifiants
pubmed: 36589675
doi: 10.1016/j.crneur.2022.100068
pii: S2665-945X(22)00041-9
pmc: PMC9800307
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100068Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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