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HDL 3 reduces the association and modulates the metabolism of oxidized LDL by osteoblastic cells: A protection against cell death
Author(s) -
Brodeur Mathieu R.,
Brissette Louise,
Falstrault Louise,
Moreau Robert
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21938
Subject(s) - association (psychology) , metabolism , programmed cell death , chemistry , microbiology and biotechnology , medicine , biochemistry , biology , apoptosis , psychology , psychotherapist
Oxidized low density lipoproteins (OxLDL) are known to promote atherosclerosis, but it is only recently that OxLDL have been associated with alterations of the functions of bone‐forming osteoblasts and osteoporosis. Although high density lipoproteins (HDL) are recognized for their anti‐atherogenic action, there is less information about their ability to protect against osteoporosis. Therefore, we investigated the capacity of HDL 3 to prevent the cell death induced by OxLDL in human osteoblastic cells. Simultaneous exposure of the cells to HDL 3 and OxLDL abolished the reduction of cell viability monitored by MTT activity measurement and the induction of apoptosis determined by annexin V staining indicating that HDL 3 prevent the apoptosis of osteoblasts induced by OxLDL. This protection correlated with the displacement by HDL 3 of OxLDL association to osteoblasts, signifying that OxLDL binding and/or internalization are/is necessary for their cytotoxic effects. We also found that exposition of osteoblastic cells to HDL 3 prior to incubation with OxLDL reduced cell death and preserved the lysosomal integrity. This protection was correlated with an increase of SR‐BI expression, a modification of OxLDL metabolism with less global uptake of OxLDL and greater selective uptake of cholesterol from OxLDL. These results strongly suggest that, as for atherosclerosis, HDL may exert beneficial actions on bone metabolism. J. Cell. Biochem. 105: 1374–1385, 2008. © 2008 Wiley‐Liss, Inc.