Download Plasminogen Activator Inhibitor Type-2 (PAI-2) - Bio

Plasminogen Activator Inhibitor Type-2
(PAI-2)
Interest in any of the products,
request or order them at Bio-Connect Diagnostics.
Bio-Connect Diagnostics B.V.
Begonialaan 3a
6851 TE Huissen
The Netherlands
T NL +31 (0)26 326 44 60
T BE +32 (0)2 502 12 53
F NL +31 (0)26 326 44 61
F BE +32 (0)2 502 12 77
E [email protected]
W www.bio-connectdiagnostics.nl
Plasminogen Activator Inhibitor Type-2
(PAI-2)
Latest scientific evidence
Maternal soluble fms-like tyrosine kinase-1, placental growth factor, plasminogen
activator inhibitor-2, and folate concentrations and early fetal size: the Generation R
study.
Bouwland-Both MI. et al., Am J Obstet Gynecol. 2013 Aug;209(2):121.e1-121.e11.
Summary:
Plasminogen activator inhibitor (PAI)-2 is a determinant of placental development, besides
fms-like tyrosine kinase (sFlt)-1, placental growth factor (PIGF) and the B vitamin folate. In
their study Bouwland-Both and colleagues analysed the association between these maternal
determinants and early fetal size. The four biomarkers including PAI-2 were found to be
positively correlated with first-trimester fetal size.
SerpinB2 is critical to Th2 immunity against enteric nematode infection.
Zhao A. et al., J Immunol. 2013 Jun 1;190(11):5779-5787.
Summary:
In this study Zhao and colleagues used PAI-2 (serpinB2) deficient mice to analyse the host
response to the enteric nematode, Heligmosomoides bakeri. Nematode infections in mice
result in increased intestinal PAI-2 expression. In PAI-2 deficient mice this up-regulation
together with concomitant IL-4 and IL-13 expression was attenuated coincident with an
impaired worm clearance. Also the nematode-induced smooth muscle hypercontractability
was lost and the infection-induced increase in mucosal permeability was delayed. In isolated
macrophages CCL2 expression was reduced. The authors conclude that “immune regulation
of serpin B2 expression plays a critical role in the development of Th2-mediated protective
immunity against nematode infection by a mechanism involving CCL2 production and
macrophage infiltration”.
Secretion of SerpinB2 from endothelial cells activated with inflammatory stimuli.
Boncela J. Et al., Exp Cell Res. 2013 May 1;319(8):1213-1219.
Summary:
PAI-2 lacks an N-terminal signal peptide and upon stimulation accumulates in cells and only a
small percentage of it is secreted. However, under inflammatory conditions the extracellular
concentration of PAI-2 increases. Boncela and colleagues explored the possible mechanism
that may underlie the secretion of PAI-2 from endothelial cells stimulated with
lipopolysaccharide (LPS). They found that stimulation generated PAI-2 containing structures
that resemble secretory vesicles. “These vesicles may represent the mechanism by which
high local concentrations of serpinB2 are released at inflammation sites from endothelial
cells.”
american diagnostica GmbH
Kaplaneigasse 35
D-64319 Pfungstadt
Tel: +49 (0)6157-99 08 99
Fax: +49 (0)6157-99 08 08
email:
[email protected]
www.americandiagnostica.de
Plasminogen Activator Inhibitor Type-2
(PAI-2)
Latest scientific evidence
Plasminogen Activator Inhibitor-2 Polymorphism Associates with Recurrent Coronary
Event Risk in Patients with High HDL and C-Reactive Protein Levels.
Corsetti JP. et al., PLoS One. 2013 Jul 9;8(7):e68920.
Summary:
Corsetti and colleagues analysed whether the PAI-2 polymorphism rs6095 is associated with
recurrent cardiac events. Indeed, Kaplan Meier analysis revealed that carriers of the variant
allele had a much higher risk of recurrent coronary events. The authors interpret this finding
in view of the possible role of PAI-2 in inhibition of plasminogen activators especially in
inflammatory foci.
TANK-binding kinase 1 (TBK1) controls cell survival through PAI-2/serpinB2 and
transglutaminase 2.
Delhase M. et al., Proc Natl Acad Sci U S A. 2012 Jan 24;109(4):E177-86.
Summary:
Delhase and colleagues addressed the fact that genetic studies in mice have identified the
TANK-binding kinase 1 (TBK1) as a regulatory molecule that promotes survival downstream
of Tumor Necrosis Factor signalling. The mechanism by which TBK1 exerts its survival
function remained elusive. In a mouse model they provided evidence for “PAI-2 and
transglutaminase 2 as downstream mediators in the anti-apoptotic response triggered upon
TBK1 activation.”
Association of plasminogen activator inhibitor type 2 (PAI-2) with proteasome within
endothelial cells activated with inflammatory stimuli.
Boncela J. et al., J Biol Chem. 2011 Dec 16;286(50):43164-43171.
Summary:
PAI-2 synthesis can be rapidly stimulated in endothelial cells by inflammatory stimuli. Boncela
and colleagues analysed the interaction between PAI-2 and proteasomes in cultured
endothelial cells. By transfection experiments together with co-immunoprecipitation as well as
electron and confocal microscopy, they provide evidence that PAI-2 interacts as an inhibitor
with proteasomes. Taken together, they suggest “that PAI-2 in endothelial cells induced with
inflammatory stimuli, can inhibit proteasome and thus tilt the balance favouring proapoptotic
signalling”.
american diagnostica GmbH
Kaplaneigasse 35
D-64319 Pfungstadt
Tel: +49 (0)6157-99 08 99
Fax: +49 (0)6157-99 08 08
email:
[email protected]
www.americandiagnostica.de