Dysregulated levels of glycogen synthase kinase-3[beta] (GSK-3[beta]) and miR-135 in peripheral blood samples of cases with nephrotic syndrome

Background Glycogen synthase kinase-3 (GSK-3[beta]) is a serine/threonine kinase with multifunctions in various physiological procedures. Aberrant level of GSK-3[beta] in kidney cells has a harmful role in podocyte injury. Methods In this article, the expression levels of GSK-3[beta] and one of its...

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Veröffentlicht in:PeerJ (San Francisco, CA) CA), 2020-12, Vol.8, p.e10377
Hauptverfasser: Ardalan, Mohammadreza, Hejazian, Seyyedeh Mina, Sharabiyani, Hassan Fazlazar, Farnood, Farahnoosh, Ghafari Aghdam, Amirhossein, Bastami, Milad, Ahmadian, Elham, Zununi Vahed, Sepideh, Cucchiarini, Magali
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Sprache:eng
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Zusammenfassung:Background Glycogen synthase kinase-3 (GSK-3[beta]) is a serine/threonine kinase with multifunctions in various physiological procedures. Aberrant level of GSK-3[beta] in kidney cells has a harmful role in podocyte injury. Methods In this article, the expression levels of GSK-3[beta] and one of its upstream regulators, miR-135a-5p, were measured in peripheral blood mononuclear cells (PBMCs) of cases with the most common types of nephrotic syndrome (NS); focal segmental glomerulosclerosis (FSGS) and membranous glomerulonephritis (MGN). In so doing, fifty-two cases along with twenty-four healthy controls were included based on the strict criteria. Results Levels of GSK-3[beta] mRNA and miR-135 were measured with quantitative real-time PCR. There were statistically significant increases in GSK-3[beta] expression level in NS (P=0.001), MGN (P=0.002), and FSGS (P=0.015) groups compared to the control group. Dysregulated levels of miR-135a-5p in PBMCs was not significant between the studied groups. Moreover, a significant decrease was observed in the expression level of miR-135a-5p in the plasma of patients with NS (P=0.020), MGN (P=0.040), and FSGS (P=0.046) compared to the control group. ROC curve analysis approved a diagnostic power of GSK-3[beta] in discriminating patients from healthy controls (AUC: 0.72, P=0.002) with high sensitivity and specificity. Conclusions Dysregulated levels of GSK-3[beta] and its regulator miR-135a may participate in the pathogenesis of NS with different etiology. Therefore, more research is needed for understanding the relationship between them.
ISSN:2167-8359
2167-8359
DOI:10.7717/peerj.10377