PMID- 17908330
OWN - NLM
STAT- MEDLINE
DCOM- 20080109
LR  - 20230814
IS  - 1471-2202 (Electronic)
IS  - 1471-2202 (Linking)
VI  - 8
DP  - 2007 Oct 2
TI  - Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in 
      transformed rat retinal ganglion cell line.
PG  - 81
AB  - 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.
FAU - Hong, Samin
AU  - Hong S
AD  - Institute of Vision Research, Department of Ophthalmology, Yonsei University 
      College of Medicine, Seoul, Korea. samini@yuhs.ac
FAU - Lee, Jong Eun
AU  - Lee JE
FAU - Kim, Chan Yun
AU  - Kim CY
FAU - Seong, Gong Je
AU  - Seong GJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Retracted Publication
DEP - 20071002
PL  - England
TA  - BMC Neurosci
JT  - BMC neuroscience
JID - 100966986
RN  - 0 (Neuroprotective Agents)
RN  - 70J407ZL5Q (Agmatine)
SB  - IM
RIN - BMC Neurosci. 2023 Aug 14;24(1):42. PMID: 37580650
MH  - Agmatine/*pharmacology
MH  - Animals
MH  - Apoptosis/*drug effects/physiology
MH  - Cell Differentiation/drug effects/physiology
MH  - Cell Hypoxia/drug effects/physiology
MH  - Cell Line, Transformed
MH  - Cell Survival/drug effects/physiology
MH  - Humans
MH  - Neuroprotective Agents/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Retinal Ganglion Cells/*drug effects/pathology/physiology
PMC - PMC2089075
EDAT- 2007/10/03 09:00
MHDA- 2008/01/10 09:00
PMCR- 2007/10/02
CRDT- 2007/10/03 09:00
PHST- 2007/04/03 00:00 [received]
PHST- 2007/10/02 00:00 [accepted]
PHST- 2007/10/03 09:00 [pubmed]
PHST- 2008/01/10 09:00 [medline]
PHST- 2007/10/03 09:00 [entrez]
PHST- 2007/10/02 00:00 [pmc-release]
AID - 1471-2202-8-81 [pii]
AID - 10.1186/1471-2202-8-81 [doi]
PST - epublish
SO  - BMC Neurosci. 2007 Oct 2;8:81. doi: 10.1186/1471-2202-8-81.