PTEN、MMP2和NF-κB与调节微小RNA-181加重胰岛素抵抗和糖尿病肾病进展的病例对照研究

Manoj Khokhar, P. Purohit, S. Tomo, R. Agarwal, A. Gadwal, N. Bajpai, G. Bohra, R. Shukla
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引用次数: 2

摘要

糖尿病肾病(DN)的特征是尿白蛋白排泄增加、糖尿病肾小球病变和肾小球滤过率(GFR)下降。我们评估了健康对照组(HC)、无肾病的2型糖尿病(T2DM)患者和DN患者中磷酸酶和紧张素同源物(PTEN)、核因子κ-β(NF-κB)、基质金属蛋白酶-2(MMP2)和微小RNA-181的表达。我们的研究调查了这些基因、胰岛素抵抗(IR)和eGFR之间的关系,以深入了解它们在DN发病机制和进展中的作用。对HC(N=36)、T2DM(N=38)和DN(N=35)患者进行了人体测量和生化测试。我们使用实时聚合酶链式反应(RT-PCR)进行全血基因表达分析,并进行生物信息学分析,包括蛋白质-蛋白质相互作用、基因本体论和共表达网络。我们将我们的表达数据与其他GEO微阵列数据集进行了比较。我们的研究强调了IR通过PTEN-Akt-mTOR信号通路在T2DM肾病进展中的作用。我们还观察到,随着肾病进展到严重阶段,MMP2和PTEN的表达呈下降趋势,NF-κB和miR-181b-5p的表达呈上升趋势。MMP2、PTEN、NF-κB和miR-181b-5p在T2DM患者中的表达失调,通过加重IR、炎症、加速基底膜增厚、系膜基质扩张和肾纤维化,导致T2DM向DN的进展。
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PTEN, MMP2, and NF-κB and Regulating MicroRNA-181 Aggravate Insulin Resistance and Progression of Diabetic Nephropathy: A Case-Control Study
Diabetic nephropathy (DN) is characterized by an increase in urinary albumin excretion, diabetic glomerular lesions, and a decline in glomerular filtration rate (GFR). We assessed the expression of phosphatase and tensin homolog (PTEN), nuclear factor kappa-β (NF-κB), matrix metalloproteinase-2 (MMP2), and microRNA-181 in healthy controls (HC), individuals with type 2 diabetes mellitus (T2DM) without nephropathy, and those with DN. Our study investigated the association between these genes, insulin resistance (IR), and eGFR to gain insight into their roles in the pathogenesis and progression of DN. Anthropometric measurements and biochemical tests were conducted on HC (N = 36), T2DM (N = 38) patients, and DN (N = 35) patients. We used real-time polymerase chain reaction (RT-PCR) for whole blood gene expression analysis and performed bioinformatics analyses, including protein–protein interaction, gene ontology, and co-expression networks. We compared our expression data with other GEO-Microarray datasets. Our study highlights the role of IR in the progression of nephropathy in T2DM via the PTEN-Akt-mTOR signalling pathway. We also observed a decreasing trend in the expression of MMP2 and PTEN and an increasing trend in the expression of NF-κB and miR-181b-5p with the progression of nephropathy to the severe stage. The dysregulated expression of MMP2, PTEN, NF-κB, and miR-181b-5p in patients with T2DM contributes to the progression of T2DM to DN by aggravating IR, inflammation, accelerating basement membrane thickening, mesangial matrix expansion, and renal fibrosis.
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