Resistin, TNF-α, and microRNA 124-3p expressions in peripheral blood mononuclear cells are associated with diabetic nephropathy

2021 
Diabetic nephropathy causes chronic kidney disease and renal failure globally. We investigated the mRNA expression of resistin, TNF-α, and microRNA 124-3p (miR-124-3p) in peripheral blood mononuclear cells (PBMCs) of diabetic patients with and without nephropathy. The mRNA expression of target genes in isolated PBMCs from whole blood was determined using real-time quantitative reverse transcription (RT) polymerase chain reaction (qRT-PCR). Demographic and clinical characteristics of study patients were also measured by standard methods. Relative expression of resistin and TNF-α was significantly increased (approximately 10-fold, and 1.5-fold respectively) in patients with nephropathy compared to that in patients without nephropathy (p < 0.001). However, the miR-124-3p expression was significantly decreased (approximately 10-fold) in patients with nephropathy in comparison to that in patients without nephropathy (p < 0.05). The expression of resistin was significantly associated with inflammatory markers such as creatinine, BUN, TNF-α, and miR-124-3p. The high expression of resistin was significantly associated with diabetic nephropathy (OR = 1.145; 95% C = 1.1–18.289, p = 0.024). The diagnostic performance of resistin, TNF-α, and miR-124-3p was significant based on ROC curve analysis (0.803, 95% CI: 0.723–0.926; 0.705, %95 CI: 0.559–0.851; and 0.707, 95% CI: 0.559–0.855, respectively). Thus, they can represent a diabetic biomarker for reflecting an advanced stage of the disease and inflammatory condition. Our findings indicated that high expression of resistin in PBMCs is associated with diabetic nephropathy. Additionally, we suggested that the expression of resistin, TNF-α, and miR-124-3p in PBMCs of diabetic patients may be represented as predictive biomarkers for the diagnosis of nephropathy.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    30
    References
    0
    Citations
    NaN
    KQI
    []