Endothelial and Pericyte Differentiation of Human Mesenchymal Stem Cells Were Inhibited in Diabetic Condition

Endothelial and Pericyte Differentiation of Human Mesenchymal Stem Cells Were Inhibited in Diabetic Condition


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نویسندگان: جعفر رضایی , رضا رهبرقاضی

عنوان کنگره / همایش: سومین جشنواره ملی و کنگره بین المللی علوم و فناوری سلول های بنیادی و پزشکی بازساختی , Iran (Islamic Republic) , Tehran , 2018

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نویسنده ثبت کننده مقاله رضا رهبرقاضی
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز سلولهای بنیادی
کد مقاله 65490
عنوان فارسی مقاله Endothelial and Pericyte Differentiation of Human Mesenchymal Stem Cells Were Inhibited in Diabetic Condition
عنوان لاتین مقاله Endothelial and Pericyte Differentiation of Human Mesenchymal Stem Cells Were Inhibited in Diabetic Condition
نوع ارائه پوستر
عنوان کنگره / همایش سومین جشنواره ملی و کنگره بین المللی علوم و فناوری سلول های بنیادی و پزشکی بازساختی
نوع کنگره / همایش بین المللی
کشور محل برگزاری کنگره/ همایش Iran (Islamic Republic)
شهر محل برگزاری کنگره/ همایش Tehran
سال انتشار/ ارائه شمسی 1397
سال انتشار/ارائه میلادی 2018
تاریخ شمسی شروع و خاتمه کنگره/همایش 1397/09/07 الی 1397/09/10
آدرس لینک مقاله/ همایش در شبکه اینترنت
آدرس علمی (Affiliation) نویسنده متقاضی Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

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نویسنده نفر چندم مقاله
جعفر رضاییاول
رضا رهبرقاضیپنجم

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عنوان متن
کلمات کلیدیEndothelial; Pericyte; Human mesenchymal stem cells; Diabetic Mellitus
خلاصه مقالهBackground and Aim: Human mesenchymal stem cells (hMSCs) with selfrenewal activity, trans-differentiation into different lineages contribute to the reconstitution of injured tissues by augmentation of angiogenesis. It was reported that in patients with diabetes type 2 DM2 deficient and abnormal angiogenesis are very common. hMSCs are more sensitive to the persistent diabetic condition. In the present study, we aimed to study the effect of sera from DM2 patients on the differentiation capacity of hMSCs into endothelial and pericyte cells. Methods: For in vitro assays, hMSCs were classified into three groups as follows; Control: cells received FBS; Non-diabetic: cells received sera from healthy subjects and Diabetic groups treated with diabetic sera. hMSCs were exposed to DMEM/LG containing 10% FBS, healthy and diabetic sera over a period of 7 days. To measure the differentiation capacity of hMSCs, cells were incubated with endothelial and pericytes differentiation media after 7-day exposure to FBS and sera from healthy and diabetic subjects. To monitor the endothelial- and pericyte-like differentiation, the expression of VE-cadherin (CD144) (Cat no 53-1449- 41, ebioscience) and NG2 (Cat no: 53-6504-82, ebioscience) were monitored by a flow cytometry and low-density lipoprotein (LDL) uptake assays. Data are shown as mean SD. One-way analysis of variance (ANOVA) and Tukey post hoc test was used in experiments between groups. Values of P < 0.05 were considered statistically significant. Results: Diabetic serum inhibited hMSCs differentiation capacity by down-regulating VE-cadherin as compared to cells from FBS and nondiabetic groups (P diabetic sera vs. FBS <0.000001; P diabetic sera vs. non-diabetic <0.01). The maximum level of VE-cadherin revealed in FBS group which was more than non-diabetic counterpart (P < 0.0001). In the absence of differentiation factors, 14-day incubation of hMSCs with FBS, non-diabetic and diabetic sera showed a similar pattern in the dynamic of VE-cadherin. Data from fluoresce microscopy confirmed that the potential of hMSCs in FBS and non-diabetic groups to uptake Dil- Ac-LDL after being exposed to endothelial induction medium. While the ability for uptake of Ac-LDL in differentiated cells and lipoprotein lipase activity was profoundly abolished in diabetic condition. There was a significant inhibitory effect of diabetic sera on pericyte differentiation capacity in hMSCs (P diabetic sera vs. FBS <0.001). Compared to FBS group, we also found a significant reduction in pericyte differentiation of hMSCs (P < 0.01). Conclusion: Our data revealed that DM2 could potentially decrease both endothelial and pericyte differentiation of hMSCs.

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