Disease relevance of PAI2

• Different Helicobacter pylori lipopolysaccharides (LPSs) and LPS-derivatives were studied for their ability to induce the production of procoagulant activity (PCA) and plasminogen activator inhibitor type 2 (PAI-2) by human blood mononuclear leukocytes [1].

High impact information on PAI2

• Failure of monocytes to accumulate PAI-2 did not reflect leakage due to cell death, as assessed by LDH in culture supernatants [2].
• Smooth (S)- and rough (R)-form LPSs caused a similar increase in cell-associated PCA (tissue factor) and PAI-2 antigen release [1].
• The endotoxin-induced PAI from both cell types was not immunoprecipitated by incubation with IgG directed against the endothelial-type inhibitor, PAI-1, or antiserum directed against the placental-type inhibitor, PAI-2 [3].
• Partial amino acid sequencing of the purified B-43 showed that this protein was homologous to glia-derived nexin/protease nexin-1 (GDN/PN-1), plasminogen activator inhibitor 2, leukocyte elastase inhibitor (LEI) and placental thrombin inhibitor (PTI) among the serpins [4].
• Embryonic PA activity was suppressed (P < .05) by PAI-2, whereas exposure to ouabain did not affect (P > .05) PA activity [5].

Biological context of PAI2

• Bovine mammary epithelial (BME-UV1, clone E-T and BME-UV, clone E-T2) and myoepithelial (BMM-UV, clone m-T2) cell lines were used to study the modulation of cell-associated activity of urokinase-type plasminogen activator (u-PA), as well as mRNA transcripts of u-PA, its receptor (u-PAR), and inhibitors (PAI-1 and PAI-2) during the cell cycle [6].
• Both PAI-1 and PAI-2 mRNAs were upregulated markedly after the gonadotrophin surge, with the highest expression observed in follicles collected at about the time of ovulation (24 h) and in corpora lutea (48 h) [7].
• A pattern of PAI-2 response in HGF after LPS stimulation was detected with a quick up-regulation of the PAI-2 mRNA, which was down regulated when extracellular PAI-2 (60kDa mass) levels reached plateau levels [8].

Anatomical context of PAI2

• These findings suggest that the induction of monocyte tissue factor and PAI-2 by H. pylori LPS is influenced by the lipid A structure and modulated by the core oligosaccharide and that phosphate groups present in both regions may play an important role [1].
• RESULTS: The results showed that the distribution of PAI-2 synthesised by human gingival fibroblasts (HGF) was mostly as an intracellular protein (47kDa) [8].
• In contrast, PAI-2 mRNA was localized specifically to the granulosa cell layer [7].

Associations of PAI2 with chemical compounds

• The aim of the present study was to investigate how serum factors, might modulate the effects of lipopolysaccharide (LPS) and interleukin-1beta on PAI-2 production by human gingival fibroblasts [8].

Analytical, diagnostic and therapeutic context of PAI2

• The expression of PAI-2 and its mRNA was monitored by Western blotting, RT-PCR, and Northern blotting [8].

References