Antiapoptotic Activity (antiapoptotic + activity)

Distribution by Scientific Domains


Selected Abstracts


HDL-c is a powerful lipid predictor of cardiovascular diseases

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 11 2007
E. Bruckert
Summary Relationship between HDL-c and cardiovascular diseases:, Beyond the role of low-density lipoprotein cholesterol (LDL-c) in the development of atherosclerosis, growing evidence suggest that high-density lipoprotein cholesterol (HDL-c) is a powerful predictor of cardiovascular disease. Indeed, epidemiological, mechanistic and intervention studies suggest that low HDL-c is a major cardiovascular risk factor and that increasing HDL-c plasma levels may be beneficial, particularly in patients with low HDL-c levels. The inverse association between HDL-c concentrations and cardiovascular risk is continuous without threshold value. Thus, any categorical definition of low HDL-c is arbitrary. Protective effects of HDL:, HDL particles are highly heterogeneous in structure and intravascular metabolism. Antiatherogenic properties of HDL include its role in the reverse cholesterol transfer, besides its antioxidant, anti-inflammatory and antiapoptotic activities. What should clinicians do?:, From a practical point of view, HDL-c should be systematically measured to assess the cardiovascular risk in patients. The first step to consider in subjects with low HDL-c is to look for specific causes and give advice to change inappropriate lifestyle components associated with low HDL-c, such as smoking, lack of physical exercise and overweight. Patients with very low HDL-c need a thorough evaluation by specialist physicians. Statins are associated with a modest increase of HDL-c (5%) while fibrates and nicotinic acid increase HDL-c by 10% and 20% respectively. [source]


The cytoprotective effects of addition of activated protein C into preservation solution on small-for-size grafts in rats

LIVER TRANSPLANTATION, Issue 1 2010
Naohisa Kuriyama
Small-for-size liver grafts are a serious obstacle for partial orthotopic liver transplantation. Activated protein C (APC), a potent anticoagulant serine protease, is known to have cell-protective properties due to its anti-inflammatory and antiapoptotic activities. This study was designed to examine the cytoprotective effects of a preservation solution containing APC on small-for-size liver grafts, with special attention paid to ischemia-reperfusion injury and shear stress in rats. APC exerted cytoprotective effects, as evidenced by (1) increased 7-day graft survival; (2) decreased initial portal pressure and improved hepatic microcirculation; (3) decreased levels of aminotransferase and improved histological features of hepatic ischemia-reperfusion injury; (4) suppressed infiltration of neutrophils and monocytes/macrophages; (5) reduced hepatic expression of tumor necrosis factor , and interleukin 6; (6) decreased serum levels of hyaluronic acid, which indicated attenuation of sinusoidal endothelial cell injury; (7) increased hepatic levels of nitric oxide via up-regulated hepatic endothelial nitric oxide synthesis expression together with down-regulated hepatic inducible nitric oxide synthase expression; (8) decreased hepatic levels of endothelin 1; and (9) reduced hepatocellular apoptosis by down-regulated caspase-8 and caspase-3 activities. These results suggest that a preservation solution containing APC is a potential novel and safe product for small-for-size liver transplantation, alleviating graft injury via anti-inflammatory and antiapoptotic effects and vasorelaxing conditions. Liver Transpl 16:1,11, 2010. 2009 AASLD. [source]


Upregulated claudin-1 expression confers resistance to cell death of nasopharyngeal carcinoma cells

INTERNATIONAL JOURNAL OF CANCER, Issue 6 2010
Jeng-Woei Lee
Abstract Accumulating evidence reveals that aberrant expression of claudins manifests in various tumors; however, their biological functions are poorly understood. Here, we report on the elevated expression of claudin-1 in nasopharyngeal carcinoma (NPC) cell lines under serum deprivation or fluorouracil (5-FU) treatment. Interestingly, an increase in expression of claudin-1 considerably reduced apoptosis rather than enhancing cell proliferation. However, claudin-1 expression and activity were unaffected by external stimuli or Akt and NF-,B activation. Notably, predominant cytoplasmic and nuclear localization of claudin-1 in NPC cells reflected the aforementioned feature. On the other hand, loss of epithelial morphology and E-cadherin expression was associated with serum withdrawal in NPC cells. Interestingly, restoration of E-cadherin inhibited the protein elevation and antiapoptotic activity of claudin-1. In conclusion, our data demonstrate the regulation and novel biological function of claudin-1 and indicate the important role of claudin-1 in NPC tumorigenesis. [source]


Effect of adiponectin on apoptosis: Proapoptosis or antiapoptosis?

BIOFACTORS, Issue 3 2010
Yiyi Sun
Abstract Adiponectin is a protein hormone mainly secreted by adipose tissue that regulates energy homeostasis and glucose and lipid metabolism. Compared with other adipose-derived hormones, adiponectin is very abundant in plasma and is proposed to be a convenient biomarker for many diseases. A large number of in vitro and in vivo studies support the beneficial effects of adiponectin on metabolic syndrome, diabetes, and atherosclerosis. However, the protective actions were challenged occasionally by the controversies in its role in inflammation and in the specific functions of its different conformations. Recently, quite a few reports suggested that the antiapoptotic activity of adiponectin might contribute to its therapeutic potential during ischemia/reperfusion injury in vivo, whereas some studies demonstrated that adiponectin induced apoptosis both in vitro and in vivo. Herein, this review attempts to summarize the present consensus and divergence and to provide possible alternative and/or complementary explanations for this apparent paradox. [source]


Introduction of Clusterin Gene into Human Renal Cell Carcinoma Cells Enhances Their Resistance to Cytotoxic Chemotherapy through Inhibition of Apoptosis both in vitro and in vivo

CANCER SCIENCE, Issue 11 2001
Isao Hara
Recent studies have revealed the powerful antiapoptotic activity of clusterin in various malignant tumors; however, the significance of clusterin expression in the acquisition of a resistant phenotype against several kinds of treatment in human renal cell carcinoma (RCC) has not been well characterized. We, therefore, transfected the clusterin cDNA into RCC ACHN cells, that scarcely express clusterin protein, to examine whether overexpression of clusterin inhibits chemotherapy-induced apoptosis both in vitro and in vivo. Although no significant differences were observed in the in vitro growth rates between clusterin-transfected ACHN (ACHN/CL) and the vector only-transfected cell line (ACHN/Co), ACHN/CL exhibited high resistance to cisplatin treatment compared with ACHN/Co, with a greater than 5-fold higher IC50 through the inhibition of apoptotic cell death, which was demonstrated by DNA fragmentation analysis and western blotting of PARP protein. Moreover, intravenous administration of cisplatin into athymic nude mice bearing ACHN/CL tumors resulted in 2- to 3-times faster tumor growth compared with ACHN/Co tumors. These findings suggest that clusterin overexpression helps confer a chemoresistant phenotype through inhibition of apoptosis in human RCC cells. [source]