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首页> 外文期刊>Life sciences >Ganglioside GM3 inhibits the high glucose- and TGF-beta1-induced proliferation of rat glomerular mesangial cells.
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Ganglioside GM3 inhibits the high glucose- and TGF-beta1-induced proliferation of rat glomerular mesangial cells.

机译：神经节苷脂GM3抑制高葡萄糖和TGF-β1诱导的大鼠肾小球系膜细胞增殖。

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Abrupt proliferation of glomerular mesangial cells (GMCs) is a common feature in the early stage of diabetic glomerulopathy, and ganglioside GM3 (NeuAcalpha3Galbeta4Glcbeta1Cer) is thought to regulate the proliferation of many cell types. Recently, we have reported ganglioside GM3 as a modulator of glomerular hypertrophy in streptozotocin-induced diabetic rats []. This study examined whether modulation of cellular ganglioside GM3 could regulate the high glucose- and transforming growth factor-beta1 (TGF-beta1)-induced proliferation of GMCs. To pharmacologically modulate the cellular ganglioside GM3, GMCs originated from rat kidneys were cultured with exogenous ganglioside GM3 or d-threo-PDMP, an inhibitor of ganglioside synthesis, in the RPMI 1640 media containing normal (5.6 mM, NG) or high (25 mM, HG) glucose. HG, TGF-beta1 (10 ng/ml) and d-threo-PDMP (20 microM) significantly stimulated the mesangial cell proliferation, whereas these increments were remarkable attenuated by exogenous ganglioside mixture (0.1-0.2 mg/ml) or GM3 (20-100 microM) in a dose-dependent manner. The mesangial cell proliferation caused by HG, TGF-beta1 and d-threo-PDMP was closely correlated with decreases in both cellular sialic acid contents and ganglioside GM3 synthase activity. Based upon the mobility on high-performance thin-layer chromatography (HPTLC), GMCs showed a complex pattern of ganglioside expression that consisted, at least, of five different components of gangliosides, mainly ganglioside GM3. HG, TGF-beta1 and d-threo-PDMP induced a significant reduction of ganglioside expression with apparent changes in the composition of ganglioside GM3, and semi-quantitative analysis by HPTLC showed that ganglioside GM3 expression reduced to about 35-54% of control. These results provide a pathophysiological link between mesangial cell proliferation and ganglioside GM3 expression, indicating that exogenously added ganglioside GM3 inhibits the high-ambient glucose- and TGF-beta1-induced proliferation of cultured GMCs.
机译：肾小球系膜细胞（GMCs）的突然增殖是糖尿病性肾小球病早期的一个常见特征，神经节苷脂GM3（NeuAcalpha3Galbeta4Glcbeta1Cer）被认为可以调节许多细胞类型的增殖。最近，我们报道了神经节苷脂GM3作为链脲佐菌素诱导的糖尿病大鼠肾小球肥大的调节剂[]。这项研究检查了细胞神经节苷脂GM3的调节是否可以调节高葡萄糖和转化生长因子β1（TGF-β1）诱导的GMC增殖。为了从药理学上调节细胞神经节苷脂GM3，在含有正常（5.6 mM，NG）或高（25 mM）的RPMI 1640培养基中，将源于大鼠肾脏的GMC与神经节苷脂合成的外源神经节苷脂GM3或d-threo-PDMP一起培养。 ，HG）葡萄糖。 HG，TGF-beta1（10 ng / ml）和d-threo-PDMP（20 microM）显着刺激肾小球系膜细胞增殖，而外源神经节苷脂混合物（0.1-0.2 mg / ml）或GM3（20则显着减弱了这些增量） -100 microM）的剂量依赖性。 HG，TGF-β1和d-苏-PDMP引起的系膜细胞增殖与细胞唾液酸含量和神经节苷脂GM3合酶活性的降低密切相关。基于高效薄层色谱（HPTLC）上的迁移率，GMC显示了神经节苷脂表达的复杂模式，该模式至少由五个不同的神经节苷脂成分组成，主要是神经节苷脂GM3。 HG，TGF-β1和d-苏-PDMP诱导神经节苷脂表达显着降低，神经节苷脂GM3的组成发生明显变化，HPTLC的半定量分析显示神经节苷脂GM3的表达降至对照的35-54％。这些结果提供了肾小球膜细胞增殖和神经节苷脂GM3表达之间的病理生理联系，表明外源添加的神经节苷脂GM3抑制了高环境葡萄糖和TGF-β1诱导的培养GMC的增殖。

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