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高葡萄糖和蛋白酶体抑制剂 MG132 对大鼠肾小球系膜细胞组蛋白 H2A 和 H2B 泛素化的影响。

Impact of high glucose and proteasome inhibitor MG132 on histone H2A and H2B ubiquitination in rat glomerular mesangial cells.

机构信息

Department of Endocrinology, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, China.

出版信息

J Diabetes Res. 2013;2013:589474. doi: 10.1155/2013/589474. Epub 2013 Apr 30.

DOI:10.1155/2013/589474
PMID:23738337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3657404/
Abstract

BACKGROUND

Hyperglycemia plays a pivotal role in the development of diabetic nephropathy (DN) and may be related to epigenetic metabolic memory. One of the most crucial epigenetic mechanisms is histone modification, which is associated with the expression of a fibrosis factor in vascular injury. Aim .In this study, we investigated the ubiquitination of histones H2A and H2B to explore the epigenetic mechanisms of DN.

MATERIALS AND METHODS

The GMCs were cultured as follows: normal group, high glucose group, mannitol group, and intervention group. After 12 hr, 24 hr, and 48 hr, histones ubiquitination, transforming growth factor-β (TGF-β), and fibronectin (FN) were measured using WB, RT-PCR, and IF.

RESULT

High glucose can induce the upregulation of FN. H2A ubiquitination in GMCs increased in high glucose group (P < 0.01), whereas it decreased significantly in intervention group (P < 0.05). In contrast, H2B ubiquitination decreased with an increasing concentration of glucose, but it was recovered in the intervention group (P < 0.05). Expression of TGF-β changed in response to abnormal histone ubiquitination.

CONCLUSIONS

The high glucose may induce H2A ubiquitination and reduce H2B ubiquitination in GMCs. The changes of histone ubiquitination may be due in part to DN by activating TGF-β signaling pathway.

摘要

背景

高血糖在糖尿病肾病（DN）的发生发展中起着关键作用，可能与表观遗传代谢记忆有关。最关键的表观遗传机制之一是组蛋白修饰，它与血管损伤中纤维化因子的表达有关。目的：本研究旨在探讨组蛋白 H2A 和 H2B 的泛素化，以探讨 DN 的表观遗传机制。

材料和方法

将 GMC 培养如下：正常组、高糖组、甘露醇组和干预组。分别在 12 小时、24 小时和 48 小时后，采用 WB、RT-PCR 和 IF 检测组蛋白泛素化、转化生长因子-β（TGF-β）和纤连蛋白（FN）的表达。

结果

高糖可诱导 FN 的上调。高糖组 GMCs 中 H2A 泛素化增加（P<0.01），而干预组则明显减少（P<0.05）。相反，随着葡萄糖浓度的增加，H2B 泛素化减少，但在干预组中得到恢复（P<0.05）。TGF-β 的表达随异常组蛋白泛素化而变化。

结论

高糖可能诱导 GMCs 中 H2A 泛素化和 H2B 泛素化减少。组蛋白泛素化的变化部分可能是由于 TGF-β 信号通路的激活导致 DN。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/dc988684409f/JDR2013-589474.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/9d4aadfeb012/JDR2013-589474.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/99dbed530ee6/JDR2013-589474.007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/9d4aadfeb012/JDR2013-589474.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/400d25b0520b/JDR2013-589474.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f48/3657404/b8586eab4f8f/JDR2013-589474.003.jpg
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