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:
https://lup.lub.lu.se/record/2221225
- author
- Bryland, Anna
LU
; Wieslander, Anders
; Carlsson, Ola
LU
; Hellmark, Thomas
LU
and Godaly, Gabriela
LU
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Diabetes & Vascular Disease Research
- volume
- 9
- issue
- 1
- pages
- 42 - 51
- publisher
- SAGE Publications
- external identifiers
-
- wos:000299721400006
- pmid:22045866
- scopus:83455258057
- pmid:22045866
- 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
- 2016-04-01 11:04:45
- date last changed
- 2023-08-31 18:05:09
@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}},
series = {{Diabetes & Vascular Disease Research}},
title = {{Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions.}},
url = {{https://lup.lub.lu.se/search/files/2362290/2363988.pdf}},
doi = {{10.1177/1479164111424297}},
volume = {{9}},
year = {{2012}},
}