Deficiency of Plasminogen Activator Inhibitor Type 2 Limits Brain Edema Formation after Traumatic Brain Injury.

Plasminogen activator inhibitor-2 (PAI-2 / SerpinB2) inhibits extracellular urokinase plasminogen activator (uPA). In physiological conditions, PAI-2 is expressed at low levels but quickly due to triggers inflammation. This is a negative regulator of fibrinolysis and serves to stabilize the clot. In this study, PAI-2 expression upregulated 25 fold in the brain tissues pericontusional at 6 hours after traumatic brain injury (TBI), with a maximum increase 87-fold at 12 h.

To investigate the potential adverse effects of PAI-2 in the process of post-traumatic secondary, man-deficiency PAI-2 (PAI-2 KO) and wild-type mice (WT) were subjected to TBI by controlled cortical impact injury. The volume of brain lesions, and inflammation of the brain is no different. Total brain volume was significantly smaller in the PAI-2 KO, showed reduced brain swelling. The water content of the brain at 24 hours post-insult was significantly smaller in the PAI-2 knockout mice.

Marker vasogenic cerebral edema showed no difference in the blood-brain barrier integrity and protein expression of blood-brain barrier (claudin-5, zonula occludens-1). Unlike the plasminogen activator inhibitor-1 (PAI-1), PAI-2 plays a limited role for the formation of brain lesions and do not affect the integrity of the blood-brain barrier. PAI-2 contributes to the formation of brain edema and because it could be a promising new targets for treating post-traumatic brain edema.

Deficiency of <em>Plasminogen</em> <em>Activator</em> <em>Inhibitor</em> Type <em>2</em> Limits Brain Edema Formation after Traumatic Brain Injury.
Deficiency of Plasminogen Activator Inhibitor Type 2 Limits Brain Edema Formation after Traumatic Brain Injury.

Plasminogen driving inhibitors two (PAI two ) on the potential of invasive cell hepatocellular carcinoma in vitro through uPA- and RB / E two F1-related mechanisms.

Plasminogen activator inhibitor 2 (PAI2) has been shown to be associated with invasive phenotype and prognosis in hepatocellular carcinoma (HCC). However, the biological role and mechanisms underlying the invasion of HCC has not been explored. This study aims to address issues.First, sub-lines in the PAI2 was stably expressed and silence established by MHCC97H and BEL7402 cell lines, respectively.

Wound healing and transwell test were applied to evaluate cell migration and invasion. Urokinase-type plasminogen activator (uPA) activity was measured using ELISA kit. Real-time RT-PCR and western blotting were used to demonstrate gene expression at the mRNA and protein level. E2F1 expression in human specimens is determined by tissue microarray-based immunohistochemical staining.The sub-lines, MHCC97H-PAI2 and BEL7402-siPAI2, successfully established.

The second sub-lines do far lower and higher strength migration and invasion, respectively, in contrast to controls. In MHCC97H-PAI2 sub-line, intra-medium uPA activity significantly decreased, while the expression of RB clearly increased, compared to the control. The BEL7402-siPAI2 sub-line is presented the opposite trend. To identify the role of RB / E2F1 pathway, we transient expressed E2F1 in MHCC97H-PAI2 sub-line, and largely reversed the inhibitory effect PAI2 on cell migration and invasion, through the set several matrix metalloproteinase and epithelial-mesenchymal transition.

In HCC specimens, E2F1 expression was much higher in the tumor than in non-tumor tissue, and significantly correlated with Edmondson-Steiner grade, overall as well as data survival.Our free tumor showed that invasive potential PAI2 inhibit HCC cells through uPA – and RB / E2F1-related mechanisms.

Cat IgG Fab2-FITC conjugate (non-immune, isotype control) purified

20002-4-F 0.1 mg
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Hamster IgG-Cy5 conjugate, isotype control (Syrian)

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Rat IgG, purified (Whole, non-immune) (isotype control)

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Rat IgG purified (isotype control)

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Rat IgG Fab fragment, purified (isotype control)

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Rat IgG (Fc) fragment, purified (isotype control)

20005-1-FC 0.5 mg
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Rat IgG (Fc)-Biotin Conjuagte (isotype control), purified

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Rat IgG1 cunonjugated (isotype control)

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20005-13-PC5 25 tests
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20005-13-PE 25 tests
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20005-14-B 100 ug
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20005-14-F 100 ug
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Rat IgG2c unonjugated (isotype control)

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20005-21-B 100 ug
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Sheep IgG-Biotin Conjugate (isotype control, non-immune), purified

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20006-2-B 0.1 mg
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20006-3 100 ug
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20007-1-5 5 mg
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Human IgG (>98%, non-immune, control, powder, azide free, bulk size)

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Human IgG-FITC conjugate (isotype control, non-immune), purified

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Human IgG Fab fragment, purified

20007-1-FAB 1 mg
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Human IgG Fab fragment-FITC Conjugate, purified

20007-1-FAB-F 0.1 mg
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Human IgG Fab fragment-HRP Conjugate, purified

20007-1-FAB-HP 0.1 mg
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Human IgG F(ab')2 fragment, purified

20007-1-FAB2 1 mg
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20007-1-FAB2-B 0.1 mg
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We show that the former PS patients who developed RPS has raised fibronectin- and reduce the level of PAI-2 is already in the early / mid-pregnancy. This deviation is even more prominent in women with PV below normal pre-pregnancy, support the development of 2-step screening program for former patients to identify high-risk groups of women who may benefit from closer scrutiny.