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Increased Calcification in Osteoprotegerin-Deficient Smooth Muscle Cells: Dependence on Receptor Activator of NF-κB Ligand and Interleukin 6
Author(s) -
Andrea Callegari,
Matthew L. Coons,
Jerry Ricks,
Michael E. Rosenfeld,
Marta Scatena
Publication year - 2014
Publication title -
journal of vascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 74
eISSN - 1423-0135
pISSN - 1018-1172
DOI - 10.1159/000358920
Subject(s) - osteoprotegerin , rankl , vascular smooth muscle , medicine , endocrinology , calcification , apolipoprotein e , receptor , chemistry , activator (genetics) , biology , disease , smooth muscle
Vascular calcification is highly correlated with cardiovascular disease morbidity and mortality. Osteoprotegerin (OPG) is a secreted decoy receptor for receptor activator of NF-κB ligand (RANKL). Inactivation of OPG in apolipoprotein E-deficient (ApoE-/-) mice increases lesion size and calcification. The mechanism(s) by which OPG is atheroprotective and anticalcific have not been entirely determined. We investigated whether OPG-deficient vascular smooth muscle cells (VSMCs) are more susceptible to mineralization and whether RANKL mediates this process.

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