早期糖腎病患的生物標誌暨微小核糖核酸 miR-30c 透過調控DDAH1及IRS1 之表現量而造成腎臟細胞纖維化之影響

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早期糖肾病患的生物标志暨微小核糖核酸 miR-30c 透过调控DDAH1及IRS1 之表现量而造成肾脏细胞纤维化之影响

The biomarker for the early stage of diabetic nephropathy and microRNA miR-30c affects kidney fibrosis through regulating expression of DDAH1 and IRS1 proteins

陈书樊 , 硕士　　导师：王志宏　　

繁体中文

糖肾病；微小核醣核酸；肾脏细胞纤维化；生物标志； diabetic nephropathy ； microRNA ； miR-30c ； DDAH1 ； IRS1 ； kidney fibrosis

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Diabetes mellitus (DM) is a chronic disease that can result in many complications in people. One majority of them is kidney disease, which may finally lead to the end-stage renal disease (ESRD). However, the precise mechanism is still unclear. Hence, the better understanding of the disease may provide us novel therapeutic targets. MicroRNA is a short non-coding RNA that plays an important role in cell growth, proliferation, differentiation and immune response. Furthermore, it also has the potential to regulate several physiological and pathological processes. We found that many specific miRNA can regulate the expression of TGF-β in the kidney. Recent studies have highlighted the importance of miRNA in the regulation of glycaemia and the reduction of hyperlipidemia in DN patients. It can also modulate the abnormal extracellular matrix thickening, and prevent the chronic kidney disease from ESRD. First, according to the values of ACR, we separated the participants into four groups, H, DN1, DN2, and DN3. We detected the serum levels of β-trophin and urine levels of NO and found that β-trophin and NO were higher in DN3 and DN4 groups than in Healthy group. In order to explore the regulation of specific genes in diabetic nephropathy patients, we used micrroarray analysis to find the miRNA, which can regulate the β-trophin and NO production. In recent study, mir-30c has been found that can downregulate the lipid synthesis and the secretion of lipoprotein. It is also associated with the NO production, inflammatory response, and apoptosis. Most importantly, we found that miR-30c strongly upregulated in the development of DN. To further investigate the role of mir-30c in renal dysfunction, we overexpressed miR-30c in the podocyte cell line (E11). Upregulation of miR-30c can inhibit the DDAH1 and IRS1 expression in transcriptional levels. Our results suggest that miR-30c may play a critical role in the DN development and blockade of miR-30c may be a potential therapeutic option in DN.

参考文献 ( 56 ) 〈TOP〉

1. Abdel-Rahman, E.M., Saadulla, L., Reeves, W.B., Awad, A.S., 2012. Therapeutic modalities in diabetic nephropathy: standard and emerging approaches. J Gen Intern Med 27, 458-468.
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2. Abu-Farha, M., Al-Khairi, I., Cherian, P., Chandy, B., Sriraman, D., Alhubail, A., Al-Refaei, F., AlTerki, A., Abubaker, J., 2016. Increased ANGPTL3, 4 and ANGPTL8/betatrophin expression levels in obesity and T2D. Lipids Health Dis 15, 181.
连结：
3. Artunc, F., Schleicher, E., Weigert, C., Fritsche, A., Stefan, N., Haring, H.U., 2016. The impact of insulin resistance on the kidney and vasculature. Nat Rev Nephrol 12, 721-737.
连结：
4. Bhatwadekar, A.D., Yan, Y., Stepps, V., Hazra, S., Korah, M., Bartelmez, S., Chaqour, B., Grant, M.B., 2015. miR-92a Corrects CD34+ Cell Dysfunction in Diabetes by Modulating Core Circadian Genes Involved in Progenitor Differentiation. Diabetes 64, 4226-4237.
连结：
6. Boffa, J.J., Lu, Y., Placier, S., Stefanski, A., Dussaule, J.C., Chatziantoniou, C., 2003. Regression of renal vascular and glomerular fibrosis: role of angiotensin II receptor antagonism and matrix metalloproteinases. J Am Soc Nephrol 14, 1132-1144.
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使用DOI作为永久连结

引用含有DOI的文献

DOI可强化引用精确性、增强学术圈连结，并给予使用者跨平台的良好使用经验，目前在全世界已有超过五千万个对象申请DOI。 如想对DOI的使用与概念有进一步了解，请参考 （ ） 。

DOI可强化引用精确性、增强学术圈连结，并给予使用者跨平台的良好使用经验，目前在全世界已有超过五千万个对象申请DOI。如想对DOI的使用与概念有进一步了解，请参考（）。