Advanced

Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions.

Bryland, Anna LU ; Wieslander, Anders; Carlsson, Ola LU ; Hellmark, Thomas LU and Godaly, Gabriela LU (2012) In Diabetes & Vascular Disease Research 9(1). p.42-51
Abstract
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... (More)
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. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes & Vascular Disease Research
volume
9
issue
1
pages
42 - 51
publisher
SAGE Publications Inc.
external identifiers
  • wos:000299721400006
  • pmid:22045866
  • scopus:83455258057
ISSN
1752-8984
DOI
10.1177/1479164111424297
language
English
LU publication?
yes
id
ac16ecc3-878e-4a6f-ab56-41f31a520115 (old id 2221225)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22045866?dopt=Abstract
date added to LUP
2011-12-02 18:55:08
date last changed
2017-03-12 03:19:09
@article{ac16ecc3-878e-4a6f-ab56-41f31a520115,
  abstract     = {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.},
  author       = {Bryland, Anna and Wieslander, Anders and Carlsson, Ola and Hellmark, Thomas and Godaly, Gabriela},
  issn         = {1752-8984},
  language     = {eng},
  number       = {1},
  pages        = {42--51},
  publisher    = {SAGE Publications Inc.},
  series       = {Diabetes & Vascular Disease Research},
  title        = {Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions.},
  url          = {http://dx.doi.org/10.1177/1479164111424297},
  volume       = {9},
  year         = {2012},
}