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Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in transformed rat retinal ganglion cell line.

Hong S, Lee JE, Kim CY, Seong GJ - BMC Neurosci (2007)

Bottom Line: Agmatine reduced phosphorylation of JNK and NF-kappaB, while BDNF suppressed phosphorylation of ERK and p38.Our 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-kappaB signaling pathways.Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. samini@yuhs.ac

ABSTRACT

Background: Agmatine 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-kappaB) 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.

Results: After 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-kappaB was not influenced by hypoxic injury, phosphorylation of these two proteins was increased. Agmatine reduced phosphorylation of JNK and NF-kappaB, while BDNF suppressed phosphorylation of ERK and p38.

Conclusion: Our 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-kappaB signaling pathways. Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.

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LDH release in RGC-5 cells. LDH release in RGC-5 cells, illustrating the neuroprotective effects of agmatine and BDNF against hypoxia for (A) 12 hours, (B) 24 hours, and (C) 48 hours. Data are shown as mean ± S.E.M. of 32 measurements. *P < 0.001.
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Figure 1: LDH release in RGC-5 cells. LDH release in RGC-5 cells, illustrating the neuroprotective effects of agmatine and BDNF against hypoxia for (A) 12 hours, (B) 24 hours, and (C) 48 hours. Data are shown as mean ± S.E.M. of 32 measurements. *P < 0.001.

Mentions: We first examined the effects of hypoxia on RGC-5 cells. As shown in Figure 1, exposure to a hypoxic environment for 12, 24, and 48 hours significantly increased release of lactate dehydrogenase (LDH) by 10.17%, 20.04%, and 52.25%, respectively (all p < 0.001), thus demonstrating time-dependent hypoxia-induced neurotoxicity.


Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in transformed rat retinal ganglion cell line.

Hong S, Lee JE, Kim CY, Seong GJ - BMC Neurosci (2007)

LDH release in RGC-5 cells. LDH release in RGC-5 cells, illustrating the neuroprotective effects of agmatine and BDNF against hypoxia for (A) 12 hours, (B) 24 hours, and (C) 48 hours. Data are shown as mean ± S.E.M. of 32 measurements. *P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2089075&req=5

Figure 1: LDH release in RGC-5 cells. LDH release in RGC-5 cells, illustrating the neuroprotective effects of agmatine and BDNF against hypoxia for (A) 12 hours, (B) 24 hours, and (C) 48 hours. Data are shown as mean ± S.E.M. of 32 measurements. *P < 0.001.
Mentions: We first examined the effects of hypoxia on RGC-5 cells. As shown in Figure 1, exposure to a hypoxic environment for 12, 24, and 48 hours significantly increased release of lactate dehydrogenase (LDH) by 10.17%, 20.04%, and 52.25%, respectively (all p < 0.001), thus demonstrating time-dependent hypoxia-induced neurotoxicity.

Bottom Line: Agmatine reduced phosphorylation of JNK and NF-kappaB, while BDNF suppressed phosphorylation of ERK and p38.Our 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-kappaB signaling pathways.Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. samini@yuhs.ac

ABSTRACT

Background: Agmatine 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-kappaB) 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.

Results: After 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-kappaB was not influenced by hypoxic injury, phosphorylation of these two proteins was increased. Agmatine reduced phosphorylation of JNK and NF-kappaB, while BDNF suppressed phosphorylation of ERK and p38.

Conclusion: Our 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-kappaB signaling pathways. Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.

Show MeSH
Related in: MedlinePlus