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Granja, Marcelo Gomes; Gomes Braga, Luis Eduardo; Monteiro de Oliveira, Raphael; de Mello Silva, Eliezer; Gonçalves-de-Albuquerque, Cassiano Felippe; Silva, Adriana Ribeiro; Caire de Castro-Faria-Neto, Hugo; Araujo dos Santos, Aline; Giestal-de-Araujo, Elizabeth
Biochemical and biophysical research communications, 10/2019, Letnik: 519, Številka: 1Journal Article
Trophic factors are involved in different cellular responses. Previously we demonstrated that IL-4 treatment induces an increase in retinal ganglion cell survival (RGCS) and regulates cholinergic differentiation of retinal cells in vitro. Data from literature show that IGF-1 also promotes RGCS, an effect mediated by PI-3K/AKT pathway. The aim of this study was to investigate the role of IGF-1 and IGF-1R on RGCS mediated by IL-4 treatment and the role of M1 acetylcholine receptors in this effect. Here we show that the effect of IL-4 on RGCS depends on IGF-1 and IGF-1R activation, the PI-3K/AKT and NFkB intracellular pathways and depends on M1 mAChRs activation. IGF-1 increases the levels of M1 mAChRs in 15min, 45min, 24 h and 48 h in mixed retinal cells culture, modulates the levels of IL-4, pIGF-1R, IGF-1R. IL-4 modulates IGF-1, pIGF-1R and IGF-1R levels in different time intervals. These results put in evidence a crosstalk between IL-4 and IGF-1 and a role of M1 mAChRs, IGF-1 and IGF-1R in RGCS mediated by IL-4. •IL-4 depends on IGF-1 to mediate RGCS.•The RGCS induced by IGF-1 depends on M1-mAChRs.•IGF-1 regulates the levels of M1-mAChRs.•Crosstalk between IL-4 and IGF-1 in RCC.•IL-4 treatment activates IGF-1Rs.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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