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  • Bryland, AnnaLund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine (author)

Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions.

  • Article/chapterEnglish2012

Publisher, publication year, extent ...

  • 2011-11-01
  • SAGE Publications,2012
  • electronicrdacarrier

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  • LIBRIS-ID:oai:lup.lub.lu.se:ac16ecc3-878e-4a6f-ab56-41f31a520115
  • https://lup.lub.lu.se/record/2221225URI
  • https://doi.org/10.1177/1479164111424297DOI

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  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

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  • Hyperglycaemia and glucose degradation products (GDPs) are closely associated with oxidative stress and inflammation in diabetic patients, a condition that leads to endothelial dysfunction and cardiovascular problems. We evaluated the effect of citrate and gluconate on glucose- and GDP-induced endothelial inflammation by measuring changes in viability, inflammation and function in primary human umbilical vein endothelial cells (HUVECs). The extent of apoptosis/necrosis was measured by flow cytometry and visualised with confocal microscopy by staining with annexin V or propidium iodide, respectively. Protein kinase C-βII (PKC-βII) activation was evaluated with Western blotting. Incubation with glucose (30 mM) and GDP (50 µM) significantly increased PKC-βII expression, endothelial cell death and inflammation. The addition of citrate decreased hyperglycaemia-induced apoptosis (p = 0.021), necrosis (p = 0.04) and reduced PKC-βII expression (p = 0.021) down to background levels. Citrate improved endothelial function by reducing the inflammatory markers(p = 0.01) and by decreasing neutrophil diapedesis (p = 0.012). These results suggest that citrate may have therapeutic potential by reducing hyperglycaemia-induced endothelial inflammation and abolishing endothelial dysfunction.

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  • Wieslander, Anders (author)
  • Carlsson, OlaLund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)njur-oca (author)
  • Hellmark, ThomasLund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Autoimmunitet och njursjukdomar,Forskargrupper vid Lunds universitet,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Autoimmunity and kidney diseases,Lund University Research Groups(Swepub:lu)njur-the (author)
  • Godaly, GabrielaLund University,Lunds universitet,Avdelningen för mikrobiologi, immunologi och glykobiologi - MIG,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Microbiology, Immunology and Glycobiology - MIG,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)mmb-ggo (author)
  • NjurmedicinSektion II (creator_code:org_t)

Related titles

  • In:Diabetes & Vascular Disease Research: SAGE Publications9:1, s. 42-511752-89841479-1641

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Bryland, Anna
Wieslander, Ande ...
Carlsson, Ola
Hellmark, Thomas
Godaly, Gabriela
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MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Clinical Medicin ...
and Urology and Neph ...
MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Basic Medicine
and Immunology in th ...
MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Basic Medicine
and Microbiology in ...
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Diabetes & Vascu ...
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Lund University

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