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Exp Eye Res ; 160: 1-10, 2017 07.
Artigo em Inglês | MEDLINE | ID: mdl-28419863

RESUMO

Bevacizumab, an anti-vascular endothelial growth factor (VEGF) agent, is widely used in the treatment of retinal vascular diseases. However, due to the essential role Müller cell derived-VEGF plays in the maintenance of retinal neurons and glial cells, cell viability is likely to be affected by VEGF inhibition. We therefore evaluated the effect of bevacizumab-induced VEGF inhibition on Müller cells (MIO-M1) in vitro. MIO-M1 cells were cultured for 12 or 24 h in media containing bevacizumab at 0.25 or 0.5 mg/mL. Controls were cultured in medium only. Cell viability was determined with the trypan blue exclusion test and MTT assay. Caspase-3, beclin-1, glial fibrillary acidic protein (GFAP) and vimentin content were quantified by immunohistochemistry. Gene expression was evaluated by real-time quantitative PCR. Treatment with bevacizumab did not reduce MIO-M1 cell viability, but increased metabolic activity at 24 h (0.5 mg/mL) and induced apoptosis and autophagy, as shown by the increased caspase-3 levels at 12 h (0.25 and 0.5 mg/mL) and the increased beclin levels at 24 h (0.5 mg/mL). Caspase-3 mRNA was upregulated at 12 h and downregulated at 24 h in cells treated with bevacizumab at 0.25 mg/mL. Bevacizumab treatment was also associated with structural protein abnormalities, with decreased GFAP and vimentin content and upregulated GFAP and vimentin mRNA expression. Although bevacizumab did not significantly affect MIO-M1 cell viability, it led to metabolic and molecular changes (apoptosis, autophagy and structural abnormalities) suggestive of significant cellular toxicity.


Assuntos
Bevacizumab/farmacologia , Células Ependimogliais/patologia , Regulação da Expressão Gênica , Proteína Glial Fibrilar Ácida/genética , RNA/genética , Vimentina/genética , Inibidores da Angiogênese/farmacologia , Apoptose , Sobrevivência Celular , Células Cultivadas , Células Ependimogliais/efeitos dos fármacos , Proteína Glial Fibrilar Ácida/biossíntese , Humanos , Estresse Oxidativo , Reação em Cadeia da Polimerase em Tempo Real , Doenças Retinianas/tratamento farmacológico , Doenças Retinianas/genética , Doenças Retinianas/patologia , Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores , Vimentina/biossíntese
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