Elevated Expression of Vascular Adhesion Molecule-1, Plasminogen Activator Inhibitor-1, Cyclooxygenase-2, and Thrombomodulin in Human Umbilical Vein Endothelial Cells from Hospitalized Gestational Diabetes Mellitus Patients.
August 7, 2020

Elevated Expression of Vascular Adhesion Molecule-1, Plasminogen Activator Inhibitor-1, Cyclooxygenase-2, and Thrombomodulin in Human Umbilical Vein Endothelial Cells from Hospitalized Gestational Diabetes Mellitus Patients.

By Alyssa

protein expression in human umbilical vein endothelial cells (HUVECs) is a useful indicator of the condition of the mother during pregnancy and the intrauterine environment. Therefore, we examined the protein expression in HUVECs were obtained from patients with gestational diabetes mellitus (GDM). HUVECs were made from the umbilical cord and control GDM patients undergoing planned caesarean section between 2013 and 2014 at Teikyo University Hospital (Tokyo, Japan).

There was no difference in blood glucose levels between patients with GDM and control the time of entry. However, body mass index, pre-pregnancy (BMI) were higher in GDM patients, although changes in pregnancy BMI smaller during hospitalization. To evaluate the state of the endothelium, we examined the protein expression levels of vascular adhesion molecule-1 (VCAM-1), an adhesion molecule-1, thrombomodulin (TM), endothelial nitric oxide synthase, plasminogen activator inhibitor-1 (PAI- 1), siklooksigenase- 2 (COX-2), and VE-cadherin, which is changed by various factors in the endothelial tissue.

VCAM-1, PAI-1 and COX-2 expression was higher in HUVECs of patients with GDM compared to controls. Due to pre-pregnancy BMI was higher in patients with GDM, we examined the relationship between BMI and protein expression. However, the protein expression levels are not correlated with pre-pregnancy BMI and higher in HUVECs of GDM patients than other BMI of BMI-matched controls.

Interestingly, the expression of TM was also higher in HUVECs of BMI-matched patients with GDM. Thus, the expression of VCAM-1, PAI-1, COX-2, and TM may reflect certain factors are altered intrauterine environment in GDM patients hospitalized with weight under control.

Elevated Expression of Vascular Adhesion Molecule-1, <em>Plasminogen</em> <em>Activator</em> <em>Inhibitor</em>-1, Cyclooxygenase-<em>2</em>, and Thrombomodulin in Human Umbilical Vein Endothelial Cells from Hospitalized Gestational Diabetes Mellitus Patients.
Elevated Expression of Vascular Adhesion Molecule-1, Plasminogen Activator Inhibitor-1, Cyclooxygenase-2, and Thrombomodulin in Human Umbilical Vein Endothelial Cells from Hospitalized Gestational Diabetes Mellitus Patients.

Plasminogen driving inhibitors – two the development of excess bladder cancer support ( two PAI- ) in PAI-1 knockout mice in N-butyl-N- (4-hydroxybutyl) -nitrosamine- induced rat model of bladder cancer.

Collecting evidence suggests that the plasminogen activator inhibitor-1 (PAI-1) play an important role in bladder tumorigenesis by regulating the cell cycle. However, it remains unclear whether and how the inhibition of PAI-1 Pressing bladder tumorigenesis.To explain the therapeutic effect of PAI-1 inhibition, we tested the tumorigenicity in PAI-1 knockout (KO) mice exposed to bladder known carcinogen.PAI- 1 deficiency is not inhibit carcinogen-induced bladder cancer in carcinogen-exposed rats although wild-type mice significantly increased PAI-1 levels in bladder tissue, plasma and urine.

We found that PAI-1 KO mice exposed to carcinogens tend to upregulate protein C inhibitor (PAI-3), urokinase-type plasminogen activator (uPA) and tissue-type PA (TPA), and significantly increased PAI-2, indicating the potential compensation function of these molecules when PAI-1 was canceled. subsequent studies using gene expression microarray using bladder tissue of mice followed by post hoc bioinformatics analysis and validation experiments by qPCR and IHC showed that SERPING1 subsequently downregulated in PAI-1 KO mice exposed to BBN, suggesting that SERPING1 as a potential factor is missing which regulate PAI – 2 excess (track compensation) .

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This result indicates that the compensation serpin lanes, particularly PAI-2 overproduction in this model, support the development of bladder cancer when oncoprotein PAI-1 is deleted. Further investigation into the PAI-1 is required to identify the true potential targets for therapy of bladder cancer.