کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6002248 | 1182966 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The hyperglycemic byproduct methylglyoxal impairs anticoagulant activity through covalent adduction of antithrombin III
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
MGO concentration-dependently attenuated inhibition of thrombin and factor Xa by ATIII in PBS-based assays, both in the presence and absence of heparin. In addition, MGO concentration-dependently inhibited ATIII activity in a plasma-based system, to the level of plasma completely deficient in ATIII, again both in the presence and absence of heparin. Results from LC-MS/MS experiments revealed that MGO covalently adducts the active site Arg 393 of ATIII through two distinct glyoxalation mechanisms. We posit that active site adduction is the mechanism of MGO-mediated inhibition of ATIII, and thus contributes to the underlying pathophysiology of the diabetic hypercoagulable state and complications thereof.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Thrombosis Research - Volume 134, Issue 6, December 2014, Pages 1350-1357
Journal: Thrombosis Research - Volume 134, Issue 6, December 2014, Pages 1350-1357
نویسندگان
Richard Jacobson, Nicholas Mignemi, Kristie Rose, Lynda O'Rear, Suryakala Sarilla, Heidi E. Hamm, Joey V. Barnett, Ingrid M. Verhamme, Jonathan Schoenecker,