Glucocorticoid receptors and their upstream epigenetic regulators in adults with steroid-resistant nephrotic syndrome

Glucocorticoid receptors and their upstream epigenetic regulators in adults with steroid-resistant nephrotic syndrome


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دانشگاه علوم پزشکی تبریز
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نویسندگان: یلدا رهبرسعادت , سیده مینا حجازیان , زیبا نریمان صالح فام , میلاد بسطامی , محمد رضا اردلان , سپیده زنونی واحد

کلمات کلیدی: Nephrotic syndrome, FSGS, MGN, MicroRNAs, Glucocorticoid receptors.

نشریه: 4571 , - , - , 2020

اطلاعات کلی مقاله
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نویسنده ثبت کننده مقاله سپیده زنونی واحد
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز تحقیقات کلیه
کد مقاله 73620
عنوان فارسی مقاله Glucocorticoid receptors and their upstream epigenetic regulators in adults with steroid-resistant nephrotic syndrome
عنوان لاتین مقاله Glucocorticoid receptors and their upstream epigenetic regulators in adults with steroid-resistant nephrotic syndrome
ناشر 8
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ بلی
عنوان نشریه (خارج از لیست فوق)
نوع مقاله Original Article
نحوه ایندکس شدن مقاله ایندکس شده سطح یک – ISI - Web of Science
آدرس لینک مقاله/ همایش در شبکه اینترنت

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Steroid-resistant nephrotic syndrome (SRNS) is a clinical challenge with variable clinical outcomes. In patients with SRNS, unsuccessful anti-inflammatory and anti-proteinuric effects of steroids lead to end-stage renal disease (ESRD). Our objective was to define the expression pattern of the glucocorticoid receptors (GCR) α and β and their epigenetic regulators (miR-24, miR-30a, and miR-370) in a group of adults with SRNS. In this regard, sixty primary NS patients with focal segmental glomerulosclerosis (FSGS, N=30) and membranous glomerulonephritis (MGN, N=30) and also healthy volunteers (N=26) were enrolled. Real-time PCR was performed to evaluate the expression levels of the aforementioned genes in peripheral blood mononuclear cell (PBMC) samples. Furthermore, an in-silico analysis was performed to understand the signaling pathways and biological procedures that may be targeted by these microRNAs in NS. The decreased and increased levels of GRα and GRβ were not significant, respectively. Statistically significant reduced miR-24 levels were observed between control/MGN (P=0.022) and MGN/FSGS (P=0.032) groups. Additionally, a decrease was detected in miR-30a between MGN and FSGS (P=0.049) groups. There was a significant increase in miR-370 expression level between control and NS groups (P=0.029), as well as control/MGN (P=0.008), and MGN/FSGS (P=0.046). Bioinformatics analysis predicted the possible targets of the studied genes including genes involved in TGF-β, Notch1, and p53 signaling pathways, regulation of gene expression, intracellular signal transduction, negative regulation of response to the stimulus, cell-cell signaling, and cell activation in the pathogenesis of SRNS. Taken all together, dysregulated levels of GCRα, GCRβ were not attributed to SRNS in our patients. It seems that pharmacokinetics and the genetic variations in podocyte-related genes may be associated with the steroid-resistance in our adult patients with NS rather than GCR expression.

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نویسنده نفر چندم مقاله
یلدا رهبرسعادتاول
سیده مینا حجازیاندوم
زیبا نریمان صالح فامسوم
میلاد بسطامیچهارم
محمد رضا اردلانهفتم
سپیده زنونی واحدهشتم

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Glucocorticoid receptors and their upstream epigenetic.pdf1399/07/192637786دانلود