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Cytotoxic role of methylglyoxal in rat retinal pericytes: Involvement of a nuclear factor-kappaB and inducible nitric oxide synthase pathway.

Abstract：

:Methylglyoxal (MGO), a cytotoxic metabolite, is produced from glycolysis. Elevated levels of MGO are observed in a number of diabetic complications, including retinopathy, nephropathy and cardiomyopathy. Loss of retinal pericyte, a hallmark of early diabetic retinal changes, leads to the development of formation of microaneurysms, retinal hemorrhages and neovasculization. Herein, we evaluated the cytotoxic role of MGO in retinal pericytes and further investigated the signaling pathway leading to cell death. Rat primary retinal pericytes were exposed to 400muM MGO for 6h. Retinal vessels were prepared from intravitreally MGO-injected rat eyes. We demonstrated apoptosis, nuclear factor-kappaB (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) induction in cultured pericytes treated with MGO and MGO-injected retinal vessels. In MGO-treated pericytes, TUNEL-positive nuclei were markedly increased, and NF-kappaB was translocalized into the nuclei of pericytes, which paralleled the expression of iNOS. The treatment of pyrrolidine dithiocarbamate (an NF-kappaB inhibitor) or l-N6-(1-iminoethyl)-lysine (an iNOS inhibitor) prevented apoptosis of MGO-treated pericytes. In addition, in intravitreally MGO-injected rat eyes, TUNEL and caspase-3-positive pericytes were significantly increased, and activated NF-kappaB and iNOS were highly expressed. These results suggest that the increased expression of NF-kappaB and iNOS caused by MGO is involved in rat retinal pericyte apoptosis.

journal_name

Chem Biol Interact

journal_title

Chemico-biological interactions

authors

Kim J,Kim OS,Kim CS,Kim NH,Kim JS

doi

10.1016/j.cbi.2010.07.002

subject

Has Abstract

pub_date

2010-10-06 00:00:00

pages

86-93

issue

1

eissn

0009-2797

issn

1872-7786

pii

S0009-2797(10)00423-0

journal_volume

188

pub_type

杂志文章

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