Cigarette smoke-induced apoptosis of vascular endothelial cells contributes to the pathogenesis of chronic obstructive pulmonary disease. However, the mechanisms responsible for endothelial apoptosis remain poorly understood. We conducted an in vitro study to investigate whether DNA methylation is involved in smoking-induced endothelial apoptosis. Human umbilical vascular endothelial cells (HUV...

The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE) induces cell loss, cellular senescence, and extracellular matrix (ECM) synthesis in primary human retinal pigment epithelial (RPE) cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid pero...

BACKGROUND Nanomedicine studies have showed a great potential for drug delivery into the lung. In this manuscript nanostructured lipid carriers (NLC) containing Fluticasone propionate (FP) were prepared and their biocompatibility and effects in a human bronchial epithelial cell line (16-HBE) stimulated with cigarette smoke extracts (CSE) were tested. RESULTS Biocompatibility studies showed th...

Cigarette smoking is associated with systemic oxidative stress leading to an upregulation of antioxidant systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and heme oxygenase (HO)] in some tissues, but the response in the human placenta is unknown. The aim of this study was to determine the effect of cigarette smoke exposure on placental antioxidant expression in...

ular for lung endothelial cells, is disrupted by the toxic effect of chronic cigarette smoke in genetically susceptible patients, thus resulting in centrilobular emphysema. Specifically, we hypothesize that disappearance of lung alveoli resulting in centrilobular emphysema occurs by apoptosis after decreased expression or activity of lung vascular endothelial cell growth factor (VEGF) or its re...

BACKGROUND Abnormal immune responses are believed to be highly relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD). Dendritic cells provide a critical checkpoint for immunity by their capacity to both induce and suppress immunity. Although evident that cigarette smoke, the primary cause of COPD, significantly influences dendritic cell functions, little is known about th...

BACKGROUND Human rhinovirus (HRV) triggers exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Cigarette smoking is the leading risk factor for the development of COPD and 25% of asthmatics smoke. Smoking asthmatics have worse symptoms and more frequent hospitalizations compared to non-smoking asthmatics. The degree of neutrophil recruitment to the airways correlates with ...

Cigarette smoke can induce pulmonary vascular remodeling, which involves pulmonary artery smooth muscle cell (PASMC) proliferation, resulting in pulmonary hypertension in chronic obstructive pulmonary disease. FHL1 is a member of the FHL subfamily, characterized by an N‑terminal half LIM domain, followed by four complete LIM domains, and has been suggested to be critical in cell proliferation. ...

Background and Hypothesis: Xeroderma pigmentosum group C (XPC) is a DNA repair protein involved in the detection of damage caused by oxidative lesions through global genomic repair. Carcinogens, chemotherapeutics, UV-lesions require XPC. Exposure to one environmental toxin, cigarette smoke (CS), leads cancer development can worsen outcomes those with cancer, however, precise mechanisms why susc...

Previous studies indicate that the arachidonic acid-metabolizing enzymes COX-2 and 5-LOX are overexpressed during the process of colonic adenoma formation promoted by cigarette smoke. The aims of the present study were to investigate whether there exists a relationship between COX-2 and 5-LOX, and whether dual inhibition of COX-2 and 5-LOX has an anticarcinogenic effect in the colonic tumorigen...