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Multiple injections of anti-mouse β2glycoprotein 1 antibody induce FcRγ-dependent fetal growth restriction (FGR) in mice.

Abstract：

OBJECTIVES:The antiphospholipid syndrome (APS) is characterized by the presence of circulating antiphospholipid antibodies (aPLs), is a leading cause for thromboembolic events, repeated miscarriage, fetal loss and is a major risk factor for fetal growth restriction (FGR) and preeclampsia. In human, anti-β2 glycoprotein I (aβ2GPI) antibody is one of the aPLs and considered to be a specific and important marker for APS. However, pathophysiological changes induced by aβ2GPI antibodies in FGR are largely unknown. METHODS:In the present study, we developed a murine FGR model induced by multiple injections of WBCAL-1, a well-characterized mouse aβ2GPI monoclonal antibody. RESULTS:Administration of WBCAL-1, but not the isotype control antibody and saline, into pregnant mice specifically decreased the size of fetuses and placentas without affecting the number of delivered pups. Also, a significant increase in urinary albumin and electron microscopic changes, such as splitting layers of basal membranes in the placental labyrinth and rearrangement of pores in glomerular endothelial cells, were observed in WBCAL-1 treated mice. WBCAL-1 injection did not induce any changes in blood pressure and typical parameters of blood thromboembolic symptoms. Furthermore, FcRγ deficiency protected the fetuses from aβ2GPI antibody-induced injuries. CONCLUSIONS:Our present findings suggest that proteinuria is a symptom associated with APS-related FGR with placental and renal tissue injuries, and that FcRγ might be a molecular target for prevention of aβ2GPI antibody-mediated obstetrical pathologies.

journal_name

Placenta

journal_title

Placenta

authors

Kawaguchi R,Nunomura S,Umehara N,Nikaido T,Huppertz B,Tanaka T,Ra C

doi

10.1016/j.placenta.2012.03.010

subject

Has Abstract

pub_date

2012-07-01 00:00:00

pages

540-7

issue

7

eissn

0143-4004

issn

1532-3102

pii

S0143-4004(12)00141-5

journal_volume

33

pub_type

杂志文章

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