این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
صفحه اصلی
درباره پایگاه
فهرست سامانه ها
الزامات سامانه ها
فهرست سازمانی
تماس با ما
JCR 2016
جستجوی مقالات
یکشنبه 23 آذر 1404
Cell Journal
، جلد ۲۳، شماره ۲، صفحات ۱۷۴-۱۸۳
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Metformin Reduces Vascular Assembly in High Glucose-Treated Human Microvascular Endothelial Cells in An AMPK-Independent Manner
چکیده انگلیسی مقاله
Objective
The aim is to examine the effect of metformin in human microvascular endothelial cells exposed to high glucose (HG) concentration and compare them with the effects of other 5' adenosine monophosphate-activated protein kinase (AMPK) modulators under the same condition.
Materials and Methods
In this experimental study, human microvascular endothelial cells (HMECs) were treated with 15 mM metformin, 1 mM 5-aminoimidazol-4-carboxamideribonucleotide (AICAR) and 10 mM compound C in the presence of 20 mM glucose (hyperglycemic condition). Migration, invasion and proliferation were evaluated as well as the capillary-like structures formation. Moreover, the expression of angiogenic genes was assessed.
Results
Metformin significantly inhibited vessel formation and migration, although it did not change HMECs proliferation and invasion. In addition, metformin significantly reduced collagen formation as evidenced by histological staining. Concomitantly, expression of several genes implicated in angiogenesis and fibrosis, namely TGFß2, VEGFR2, ALK1, JAG1, TIMP2, SMAD5, SMAD6 and SMAD7, was slightly upregulated. Immunostaining for proteins involved in ALK5 receptor signaling, the alternative TGFß signaling pathway, revealed significant differences in SMAD2/3 expression.
Conclusion
Our data showed that metformin prevents vessel assembly in HMECs, probably through an AMPK- independent mechanism. Understanding the molecular mechanisms by which this pharmacological agent affects endothelial dysfunction is of paramount importance and paves the way to its particular use in preventing development of diabetic retinopathy and nephropathy, two processes where angiogenesis is exacerbated.
کلیدواژههای انگلیسی مقاله
AICAR, AMPK Signaling, Compound C, Endothelial cells, Metformin
نویسندگان مقاله
Carolina Silva |
.Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal;.i3S, Institute of Research and Innovation in Health, University of Porto, Porto, Portugal
Ilda Rodrigues |
.Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal
Sara Andrade |
.Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal;.i3S, Institute of Research and Innovation in Health, University of Porto, Porto, Portugal ;.IPATIMUP, Institute
Raquel Costa |
.Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal;.i3S, Institute of Research and Innovation in Health, University of Porto, Porto, Portugal
Raquel Soares |
.Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal;.i3S, Institute of Research and Innovation in Health, University of Porto, Porto, Portugal
نشانی اینترنتی
https://www.celljournal.org/article_250703_1b60a81ee9d155b9b0ed36e799ead5f8.pdf
فایل مقاله
فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده
برگشت به:
صفحه اول پایگاه
|
نسخه مرتبط
|
نشریه مرتبط
|
فهرست نشریات