SERUM FROM MAGNESIUM-DEFICIENT RATS AFFECTS VASCULAR ENDOTHELIAL-CELLS IN CULTURE - ROLE OF HYPERLIPEMIA AND INFLAMMATION

Citation
Jam. Maier et al., SERUM FROM MAGNESIUM-DEFICIENT RATS AFFECTS VASCULAR ENDOTHELIAL-CELLS IN CULTURE - ROLE OF HYPERLIPEMIA AND INFLAMMATION, Journal of nutritional biochemistry, 9(1), 1998, pp. 17-22
Citations number
47
Categorie Soggetti
Nutrition & Dietetics",Biology
ISSN journal
09552863
Volume
9
Issue
1
Year of publication
1998
Pages
17 - 22
Database
ISI
SICI code
0955-2863(1998)9:1<17:SFMRAV>2.0.ZU;2-6
Abstract
Magnesium (Mg) deficit has been implicated as a risk for atheroscleros is. An important characteristic of experimental Mg deficiency in mts i s the spontaneous inflammation with marked leukocytosis and increase i n plasma concentrations of inflammatory cytokines. This deficiency is also accompanied by hyperlipemia resulting from accumulation of trigly ceride-rich lipoproteins (TGRLP). The present investigation was perfor med to determine the effect of serum from Mg-deficient animals on cult ured vascular endothelial cells. Sera were obtained from control and M g-deficient rats fed for 8 days adequate or Mg-deficient diets. Mg-def icient animals presented an important leukocytosis and an increased in terleukin (IL) 6 concentration in the plasma. Deficient ma were hypert riglyceridemic as compared with control ones, but their cholesterolemi a was not modified significantly. Pooled sera from control and Mg-defi cient animals were added to the culture medium of human umbilical endo thelial cells (HUVEC). The results show that serum from Mg-deficient r ats stimulates proliferation of cultured endothelial cells, increases adhesion of monocytes to these cells, and causes an induction of plasm inogen activator inhibitor factor I (PAI-1) mRNA level in these cells. The present study demonstrates that the inflammatory and hyperlipemic serum from Mg-deficient animals affects various processes in endothel ial cells, which are known to be implicated in atherogenesis. (C) Else vier Science Inc, 1998.