کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5501037 | 1534621 | 2017 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dual role of MUC1 mucin in kidney ischemia-reperfusion injury: Nephroprotector in early phase, but pro-fibrotic in late phase
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کلمات کلیدی
RPTECsCDTAKIMUC1EGFRATNdFG - DFGacute kidney injury - آسیب حاد کلیهsmooth muscle actin - آکنه عضله صافperiodic acid-Schiff - اسید فسفریک Schiffmesenchymal-epithelial transition - انتقال مزانشیمال-اپیتلیالHES - او هستischemia-reperfusion - ایسکمی-رپرفیوژنImmunofluorescence - ایمونوفلورسانسImmunohistochemistry - ایمونوهیستوشیمیIHC - ایمونوهیستوشیمیempty vector - بردار خالیchronic kidney disease - بیماری مزمن کلیویEMT - تکنسین فوریتهای پزشکیSMA - دبیرستانFibrosis - فیبروز یا فساد الیافMET - ملاقات کردestimated glomerular filtration rate - میزان تصفیه گلومرولی برآورد شده استCKD - نارسایی مزمن کلیهknockout - ناکاوتPAS - نهwild-type - نوع وحشیAcute tubular necrosis - نکروز لوله ای حادCollecting ducts - کانال های جمع آوری شدهEpithelial-mesenchymal transition - گذار اپیتلیال-مزانشیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Acute kidney injury (AKI) is characterized by acute tubular necrosis (ATN) which involves mainly proximal tubules. Past AKI is associated with higher risk of chronic kidney disease (CKD). The MUC1 mucin is a large glycoprotein responsible for epithelial protection and locates to convoluted distal tubules and collecting ducts. Since MUC1 activates the epithelial-mesenchymal transition (EMT) in carcinoma cells, we hypothesized that MUC1 could be involved in epithelial tubular cell plasticity, a process that not only accompanies epithelial repair, but also participates into kidney fibrosis, histological substratum of CKD. In cultured human proximal cells and in human kidney allograft biopsies, we observed MUC1 induction in proximal tubules displaying ATN. Transient MUC1 induction localized with mesenchymal and stem-cell markers and was associated in vitro with reduced anoikis. In a mouse ischemia-reperfusion (IR) model, Muc1 expression mitigates severe tubular injury, as WT displayed less ATN than Muc1 KO mice. But, WT mice displayed more severe kidney fibrosis than Muc1 KO 28Â days after ischemia. Besides, sustained Muc1 expression in WT was associated with less kidney M2 macrophages. Human kidney biopsies performed within the first week (W1) of transplantation in the context of IR showed MUC1 W1 induction associated with EMT markers. Protocol biopsies performed 3Â months after demonstrated sustained abnormal MUC1 induction in atrophic tubules within kidney fibrosis. Altogether these data showed that sustained abnormal MUC1 induction accompanies failing epithelial repair, chronic inflammation and kidney fibrosis. In conclusion, MUC1 exerts opposite effects during kidney response to IR: first protective and then harmful.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 6, June 2017, Pages 1336-1349
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 6, June 2017, Pages 1336-1349
نویسندگان
Jean-Baptiste Gibier, Brigitte Hémon, Mélanie Fanchon, Kelly Gaudelot, Nicolas Pottier, Bélinda Ringot, Isabelle Van Seuningen, François Glowacki, Christelle Cauffiez, David Blum, Marie-Christine Copin, Michaël Perrais, Viviane Gnemmi,