کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5652418 1588889 2017 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Membrane complement regulatory protein reduces the damage of transplanting autologous bone marrow mesenchymal stem cells by suppressing the activation of complement
ترجمه فارسی عنوان
پروتئین پروتئینی حاوی پروتئین غشایی باعث آسیب رساندن سلول های بنیادی مزانشیمی مغز استخوان اتولوگ به سلول های سرطانی شده توسط مهار فعال سازی مکمل
کلمات کلیدی
غشاء مکمل پروتئین تنظیم کننده سلول های بنیادی مزانشیمی مغز استخوان، متمم، پیوند اتولوگ
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی طب اورژانس
چکیده انگلیسی
There are few studies on the interaction of transplanting autologous bone marrow mesenchymal stem cells (BMSCs) and complement. In order to further explore the effect of complement on BMSCs, BMSCs were obtained from bone marrow of 20 cases clinical patients, and then experimented in vitro. The cytotoxicity of complement on the mesenchymal stem cells in autologous human serum (AHS) was measured by Europium cytotoxicity assay. The complement membrane attack complex (MAC) deposited on the membrane surface was detected by flow cytometry. Finally, the cytotoxicity on BMSCs was measured after mCRPs overexpression or knockdown. We found that more than 90% of cells derived from bone marrow were identified to be mesenchymal stem cells through detection of cell membrane surface markers by flow cytometry. BMSCs harvested from the 20 patients all had cytotoxicity after incubated with AHS, and the cytotoxicity was significant higher than that incubated with complement inactivated autologous human serum (iAHS). Complement attack complex (MAC) could be detected on the BMSCs incubated with AHS, which implied the complement activation. We also found that mCRPs CD55 and CD59 overexpressions can resist the cytotoxicity induced by complement activation, while mCRPs CD55 and CD59 knockdown can enhance the cytotoxicity. Thus, the results indicated that mCRPs could effectively protect BMSCs from attacking by complement by suppressing the activation of complement.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Injury - Volume 48, Issue 10, October 2017, Pages 2089-2094
نویسندگان
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