Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in transformed rat retinal ganglion cell lineReportar como inadecuado




Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in transformed rat retinal ganglion cell line - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

BMC Neuroscience

, 8:81

First Online: 02 October 2007Received: 03 April 2007Accepted: 02 October 2007

Abstract

BackgroundAgmatine is an endogenous polyamine formed by the decarboxylation of L-arginine. We investigated the protective effects of agmatine against hypoxia-induced apoptosis of immortalized rat retinal ganglion cells RGC-5. RGC-5 cells were cultured in a closed hypoxic chamber 5% O2 with or without agmatine. Cell viability was determined by lactate dehydrogenase LDH assay and apoptosis was examined by annexin V and caspase-3 assays. Expression and phosphorylation of mitogen-activated protein kinases MAPKs; JNK, ERK p44-42, and p38 and nuclear factor-kappa B NF-κB were investigated by Western immunoblot analysis. The effects of agmatine were compared to those of brain-derived neurotrophic factor BDNF, a well-known protective neurotrophin for retinal ganglion cells.

ResultsAfter 48 hours of hypoxic culture, the LDH assay showed 52.3% cell loss, which was reduced to 25.6% and 30.1% when agmatine and BDNF were administered, respectively. This observed cell loss was due to apoptotic cell death, as established by annexin V and caspase-3 assays. Although total expression of MAPKs and NF-κB was not influenced by hypoxic injury, phosphorylation of these two proteins was increased. Agmatine reduced phosphorylation of JNK and NF-κB, while BDNF suppressed phosphorylation of ERK and p38.

ConclusionOur results show that agmatine has neuroprotective effects against hypoxia-induced retinal ganglion cell damage in RGC-5 cells and that its effects may act through the JNK and NF-κB signaling pathways. Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2202-8-81 contains supplementary material, which is available to authorized users.

Download fulltext PDF



Autor: Samin Hong - Jong Eun Lee - Chan Yun Kim - Gong Je Seong

Fuente: https://link.springer.com/







Documentos relacionados