Effect of methylglyoxal on intracellular calcium levels and viability in renal tubular cells

Jan, Chung‐Ren; Chen, Ching‐Hsein; Wang, Shu-Ching; Kuo, Soong-Yu

doi:10.1016/j.cellsig.2004.11.007

Cited by 47 publications

(38 citation statements)

References 29 publications

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“…A few studies have already proved that short-and long-term MG treatment of different non-neuronal cells is inducing changes in [Ca 2? ] i (Jan et al 2005;Chan and Wu 2008;Hsieh and Chan 2009). High glucose and long-term MG (24 h) co-treatment of human mononuclear cells and human umbilical vein endothelial cells increase [Ca 2? ]…”

Section: Discussionmentioning

confidence: 97%

“…At higher MG doses (250-1,000 lM), a dosedependent drop in the cell survival occurs. MG-induced apoptotic death is cell type dependent: it induces apoptosis in human umbilical vein endothelial cells (Chan and Wu 2008), Madin-Darby canine kidney renal tubular cells (Jan et al 2005), human mononuclear cells (Hsieh and Chan 2009), Neuro-2A neuroblastoma (Huang et al 2008), SH-SY5Y neuroblastoma (Li et al 2011), Jurkat (Du et al 2000) cells, rat hippocampal (Di Loreto et al 2008, and cortical neurons (Kikuchi et al 1999), but it fails to induce apoptosis in MOLT-4, HeLa, or COS-7 cells (Du et al 2000). An apoptotic death of the peripheral sensory neurons in the presence of MG might be very likely to occur.…”

Section: Discussionmentioning

confidence: 99%

“…influx and CCCP (carbonylcyanide m-chlorophenylhydrazone)-sensitive intracellular Ca 2? release, and causing apoptotic cell death (Jan et al 2005).…”

Section: Discussionmentioning

confidence: 99%

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Dual Effect of Methylglyoxal on the Intracellular Ca2+ Signaling and Neurite Outgrowth in Mouse Sensory Neurons

et al. 2012

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The formation of advanced glycation end products is one of the major factors involved in diabetic neuropathy, aging, and neurodegenerative diseases. Reactive carbonyl compounds, such as methylglyoxal (MG), play a key role in cross-linking to various proteins in the extracellular matrix, especially in neurons, which have a high rate of oxidative metabolism. The MG effect was tested on dorsal root ganglia primary neurons in cultures from adult male Balb/c mice. Lower MG doses contribute to an increased adherence of neurons on their support and an increased glia proliferation, as proved by MTS assay and bright-field microscopy. Time-lapse fluorescence microscopy by Fura-2 was performed for monitoring the relative fluorescence ratio changes (ΔR/R(0)) upon depolarization and immunofluorescence staining for quantifying the degree of neurites extension. The relative change in fluorescence ratio modifies the amplitude and dispersion depending on the subtype of sensory neurons, the medium-sized neurons are more sensitive to MG treatment when compared to small ones. Low MG concentrations (0-150 μM) increase neuronal viability, excitability, and the capacity of neurite extension, while higher concentrations (250-750 μM) are cytotoxic in a dose-dependent manner. In our opinion, MG could be metabolized by the glyoxalase system inside sensory neurons up to a threshold concentration, afterwards disturbing the cell equilibrium. Our study points out that MG has a dual effect concentration dependent on the neuronal viability, excitability, and neurite outgrowth, but only the excitability changes are soma-sized dependent. In conclusion, our data may partially explain the distinct neuronal modifications in various neurodegenerative pathologies.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Dual Effect of Methylglyoxal on the Intracellular Ca2+ Signaling and Neurite Outgrowth in Mouse Sensory Neurons

et al. 2012

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“…Ramifications of pathological MG concentrations include modulation of immune cell functions by stimulation of cytokine induction [13], activation of macrophages [14], and suppression of T-cell functions [15]. MG alters cellular functions by influencing energy and redox balance [16], modulating cytosolic Ca 2+ [17] and by triggering apoptotic or necrotic cell death [11,18].…”

Section: Introductionmentioning

confidence: 99%

Endothelial Na + /H + exchanger NHE1 participates in redox-sensitive leukocyte recruitment triggered by methylglyoxal

Qadri

Shao‐Horn

Cayabyab

et al. 2014

Cardiovasc Diabetol

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Background: Excessive levels of methylglyoxal (MG) encountered in diabetes foster enhanced leukocyte-endothelial cell interactions, mechanisms of which are incompletely understood. MG genomically upregulates endothelial serum-and glucocorticoid-inducible kinase 1 (SGK1) which orchestrates leukocyte recruitment by regulating the activation and expression of transcription factors and adhesion molecules. SGK1 regulates a myriad of ion channels and carriers including the Na

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“…However, exposure for 6 hours to 3 µM methylglyoxal had little effect on forward scatter, suggesting that at those concentrations and exposure times methylglyoxal did not substantially increase cytosolic Ca 2+ activity. At higher concentrations methylglyoxal even activity in MDCK cells [63]. Methylglyoxal is at least partially effective by an effect on glucose metabolism.…”

Section: Discussionmentioning

confidence: 95%

Stimulation of Suicidal Erythrocyte Death by Methylglyoxal

Nicolay

Schneider

Niemoeller

et al. 2006

Cell Physiol Biochem

217

178

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Diabetes increases the percentage of circulating erythrocytes exposing phosphatidylserine (PS) at the cell surface. PS-exposing erythrocytes are recognized, bound, engulfed and degraded by macrophages. Thus, PS exposure, a feature of suicidal erythrocyte death or eryptosis, accelerates clearance of affected erythrocytes from circulating blood. Moreover, PS-exposing erythrocytes bind to the vascular wall thus interfering with microcirculation. The present study explored mechanisms involved in the triggering of PS exposure by methylgloxal, an extra- and intracellular metabolite which is enhanced in diabetes. PS exposure, cell size and cytosolic Ca²⁺-activity after methylglyoxal treatment were measured by FACS analysis of annexin V binding, forward scatter and Fluo-3-fluorescence, respectively, and it was shown that the treatment significantly enhanced the percentage of PS-exposing erythrocytes at concentrations (0.3 µM) encountered in diabetic patients. Surprisingly, methylglyoxal did not significantly increase cytosolic Ca²⁺ concentration, and at concentrations up to 3 µM, did not decrease the forward scatter. Instead, exposure to methylglyoxal inhibited glycolysis thus decreasing ATP and GSH concentrations. In conclusion, methylglyoxal impairs energy production and anti-oxidative defense, effects contributing to the enhanced PS exposure of circulating erythrocytes and eventually resulting in anemia and deranged microcirculation.

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Effect of methylglyoxal on intracellular calcium levels and viability in renal tubular cells

Cited by 47 publications

References 29 publications

Dual Effect of Methylglyoxal on the Intracellular Ca2+ Signaling and Neurite Outgrowth in Mouse Sensory Neurons

Dual Effect of Methylglyoxal on the Intracellular Ca2+ Signaling and Neurite Outgrowth in Mouse Sensory Neurons

Endothelial Na + /H + exchanger NHE1 participates in redox-sensitive leukocyte recruitment triggered by methylglyoxal

Stimulation of Suicidal Erythrocyte Death by Methylglyoxal

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