کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10817112 | 1058665 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effect of methylglyoxal on intracellular calcium levels and viability in renal tubular cells
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کلمات کلیدی
Thapsigarginfura 2/AMMDCKCCCPN-acetyl-l-cysteineNACDTT1,4-dithiothreitol - 1،4-dithiothreitolFura-2 - 2-فورا[Ca2+]i - [Ca2 +] iApoptosis - خزان یاختهایDicarbonyl - دیکربنیلRenal cells - سلول های کلیهCa2+ signaling - سیگنالینگ Ca2 +endoplasmic reticulum - شبکه آندوپلاسمی intracellular Ca2+ concentration - غلظت Ca2 + داخل سلولیMethylglyoxal - متیل گلی اکسالNecrosis - نکروز یا بافتمردگیPropidium iodide - پروتئین یدیدCarbonylcyanide m-chlorophenylhydrazone - کربوکیل سایینید m-chlorophenylhydrazone
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Effect of methylglyoxal on intracellular calcium levels and viability in renal tubular cells Effect of methylglyoxal on intracellular calcium levels and viability in renal tubular cells](/preview/png/10817112.png)
چکیده انگلیسی
Methylglyoxal (2-oxopropanal), a physiological glucose metabolite, is a highly reactive dicarbonyl compound that can induce stress in cells and cause apoptotic cell death. This study examines the early signaling effects of methylglyxal on renal cells. It was found that methylglyoxal caused a slow and sustained rise of intracellular Ca2+ concentration ([Ca2+]i) in a concentration-dependent manner (EC50=1.8 mM). Methylglyoxal also induced a [Ca2+]i rise when extracellular Ca2+ was removed, but the magnitude was reduced by 80%. Depletion of intracellular Ca2+ stores with thapsigargin (TG), an endoplasmic reticulum (ER) Ca2+ pump inhibitor, did not affect methylglyoxal's effect. In Ca2+-free medium, the methylglyoxal-induced [Ca2+]i rise was abolished by depleting stored Ca2+ with carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler). Methylglyoxal-caused [Ca2+]i rise in the Ca2+-containing medium was not affected by modulation of protein kinase C activity, presence of voltage-gated Ca2+ channel blockers, or preincubation with thiol-containing antioxidants. U73122, an inhibitor of phospholipase C, abolished ATP (but not methylglyoxal)-induced [Ca2+]i rise. Furthermore, the [Ca2+]i-elevating effect of methylglyoxal was cell type-dependent, because methylglyoxal failed to cause [Ca2+]i rises in CHO-K1, neutrophils, or platelets. Pretreatment with methylglyoxal for 0-24 h decreased cell viability in a concentration- and time-dependent manner. Meanwhile, methylglyoxal-induced cell death involved apoptotic and necrotic events, the former being the dominant. These findings suggest that methylglyoxal induced a significant rise in [Ca2+]i in Madin-Darby canine kidney (MDCK) renal tubular cells by stimulating both extracellular Ca2+ influx and CCCP-sensitive intracellular Ca2+ release via as yet unidentified mechanisms. The cell type-specific Ca2+ signaling may play an important role in the early process of cytotoxic action of methylglyoxal.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 7, July 2005, Pages 847-855
Journal: Cellular Signalling - Volume 17, Issue 7, July 2005, Pages 847-855
نویسندگان
Chung-Ren Jan, Ching-Hsein Chen, Shu-Ching Wang, Soong-Yu Kuo,