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Inhibition of pericellular plasminogen activation by apolipoprotein(a): Roles of urokinase plasminogen activator receptor and integrins αMβ2 and αVβ3.

Abstract：

BACKGROUND AND AIMS:Lipoprotein(a) (Lp(a)) is a causal risk factor for cardiovascular disorders including coronary heart disease and calcific aortic valve stenosis. Apolipoprotein(a) (apo(a)), the unique glycoprotein component of Lp(a), contains sequences homologous to plasminogen. Plasminogen activation is markedly accelerated in the presence of cell surface receptors and can be inhibited in this context by apo(a). METHODS:We evaluated the role of potential receptors in regulating plasminogen activation and the ability of apo(a) to mediate inhibition of plasminogen activation on vascular and monocytic/macrophage cells through knockdown (siRNA or blocking antibodies) or overexpression of various candidate receptors. Binding assays were conducted to determine apo(a) and plasminogen receptor interactions. RESULTS:The urokinase-type plasminogen activator receptor (uPAR) modulates plasminogen activation as well as plasminogen and apo(a) binding on human umbilical vein endothelial cells (HUVECs), human acute monocytic leukemia (THP-1) cells, and THP-1 macrophages as determined through uPAR knockdown and overexpression. Apo(a) variants lacking either the kringle V or the strong lysine binding site in kringle IV type 10 are not able to bind to uPAR to the same extent as wild-type apo(a). Plasminogen activation is also modulated, albeit to a lower extent, through the Mac-1 (αMβ2) integrin on HUVECs and THP-1 monocytes. Integrin αVβ3 can regulate plasminogen activation on THP-1 monocytes and to a lesser extent on HUVECs. CONCLUSIONS:These results indicate cell type-specific roles for uPAR, αMβ2, and αVβ3 in promoting plasminogen activation and mediate the inhibitory effects of apo(a) in this process.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Romagnuolo R,Scipione CA,Bazzi ZA,Boffa MB,Koschinsky ML

doi

10.1016/j.atherosclerosis.2018.05.029

subject

Has Abstract

pub_date

2018-08-01 00:00:00

pages

11-21

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(18)30272-7

journal_volume

275

pub_type

杂志文章

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