Deamidated lipocalin-2 induces endothelial dysfunction and hypertension in dietary obese mice.

Background: Lipocalin-2 is a proinflammatory adipokine upregulated in obese humans and animals. A pathogenic role of lipocalin-2 in hypertension has been suggested. Mice lacking lipocalin-2 are protected from dietary obesity-induced cardiovascular dysfunctions.

Constitutive activation of AMPK α1 in vascular endothelium promotes high-fat diet-induced fatty liver injury: role of COX-2 induction.

Background And Purpose: AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, comprises three (α, β and γ) subunits, each with a unique tissue distribution. As AMPK has a wide range of protein and gene targets, defining its role has been difficult. Here, we have studied a transgenic mouse model overexpressing the constitutively active α1 subunit of AMPK in endothelial cells (EC-AMPK) to elucidate its role in energy homeostasis.

Selective overexpression of human SIRT1 in adipose tissue enhances energy homeostasis and prevents the deterioration of insulin sensitivity with ageing in mice.

SIRT1, a longevity regulator and NAD(+)-dependent deacetylase, plays a critical role in promoting metabolic fitness associated with calorie restriction and healthy ageing. Using a tissue-specific transgenic approach, the present study demonstrates that over-expression of human SIRT1 selectively in adipose tissue of mice prevents ageing-induced deterioration of insulin sensitivity and ectopic lipid distribution, reduces whole body fat mass and enhances locomotor activity. During ageing, the water-soluble vitamin biotin is progressively accumulated in adipose tissue.

Propofol increases angiotensin-converting enzyme 2 expression in human pulmonary artery endothelial cells.

Background/aims: Propofol, a widely used sedative-hypnotic agent for induction/maintenance of anesthesia and sedation of critically ill patients, reportedly has therapeutic potential for hypertension. Angiotensin-converting enzyme 2 (ACE2) is a promising therapeutic target for pulmonary arterial hypertension. In the present study, we explored the effect of propofol on ACE2 expression in human pulmonary artery endothelial cells (HPAECs).

A highly conserved tryptophan in the N-terminal variable domain regulates disulfide bond formation and oligomeric assembly of adiponectin.

Adiponectin is a collagenous adipokine with direct anti-diabetic and anti-atherogenic properties. It can assume an ensemble of oligomeric states, e.g.

Upregulation of UCP2 by adiponectin: the involvement of mitochondrial superoxide and hnRNP K.

Background: The adipocyte-derived hormone adiponectin elicits protective functions against fatty liver diseases and hepatic injuries at least in part by stimulating the expression of a mitochondrial inner membrane transporter, uncoupling protein 2 (UCP2). The present study was designed to investigate the cellular and molecular mechanisms underlying adiponectin-induced UCP2 expression.

Methodology/principal Findings: Mice were treated with adiponectin and/or different drug inhibitors.

Lipocalin-2 deficiency prevents endothelial dysfunction associated with dietary obesity: role of cytochrome P450 2C inhibition.

Background And Purpose: Lipocalin-2 is a pro-inflammatory adipokine up-regulated in obese human subjects and animal models. Its circulating levels are positively correlated with the unfavourable lipid profiles, elevated blood pressure and insulin resistance index. Augmented lipocalin-2 has been found in patients with cardiovascular abnormalities.

Intramembranous fragment of amyloid-beta: A potential immunogen for Alzheimer's disease immunotherapy.

Immunotherapy holds great promise for Alzheimer's disease (AD), but meningoencephalitis observed in the first AD vaccination trial, which accompanied T-lymphocytic infiltration, needs to be overcome. This study was aimed to investigate alternative approaches for a safer vaccine to treat AD. We used intramembranous fragment of amyloid-beta (IF-Abeta) to immunize Kunming mice for up to 2.

[Protection of hepatocyte growth factor on neurons subjected to oxygen-glucose deprivation/reperfusion].

The present study was conducted to investigate the effect of hepatocyte growth factor (HGF) on cortical neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R). Primary cultured cerebral cortical neurons were prepared from Sprague-Dawley rats. The cells were used for experiments after culture for 12 d in vitro.

[Protective effect of thrombin precondition on astrocytes insulted by oxygen-glucose deprivation].

Objective: To explore the effect of thrombin precondition (TPC) on the rat cerebral astrocytes(As) cultured in oxygen-glucose deprivation (OGD).

Methods: Astrocytes were pretreated with thrombin (TB) at various concentrations (0.005 approximately 5.

[Effect of thrombin on cultured rat cerebral astrocyte injured by hypoxia/reoxygenation and its relationship with iNOS].

Objective: To observe the effect of thrombin on the cytotoxicity of astrocytes injured by hypoxia/reoxygenation(H/R) and to explore its relationship with inducible nitric oxide synthase (iNOS).

Methods: Primary astrocytes were cultured in DMEM with 10% approximately 15% calf serum and divided into 6 groups: a control group, a Tm control group, an H/R group, a Tm+H/R group, a hirudin (HR) control group, and a Tm+HR+ H/R group. The cell damage and viability were detected by the 3-(4, 5-di-methyl-thazol-2-yl)-2, 5 diphenyl-tetrazol-iumbromide (MTT) conversion method.

HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways.

Hepatocyte growth factor (HGF) has been revealed to exert multipotent activities on a variety of cells. In this study, we investigated whether HGF had a direct neuroprotection on cultured cerebral cortical neurons subjected to hypoxia/reoxygenation (H/R) and explored the intracellular signalings mediated the effects. The decrease in cell viability and increase in number of apoptotic cells resulting from H/R were significantly prevented by HGF pre-treatment.