Microparticles are submicron vesicles shed from plasma membranes in response to cell activation, injury and/or apoptosis. Microparticles of various cellular origins, such as platelets, leukocytes, and endothelial cells, are found in the plasma of healthy subjects, and their amount increases under pathological conditions. Recent studies show that endothelial microparticles, a kind of envelope particles derived from endothelial cells, not only constitute a marker of endothelial dysfunction, but also play a major biological role in the diagnostic and therapeutic approaches to erectile dysfunction.
Biomarkers ; Cell Membrane ; Endothelial Cells ; metabolism ; pathology ; Erectile Dysfunction ; metabolism ; pathology ; Humans ; Liposomes ; metabolism ; Male

OBJECTIVETo observe the change in the amount of sialic acids on hepatocellular carcinoma (HCC) cell membrane.

METHODSSurgical specimens of HCC and liver cirrhosis tissues were obtained from 28 patients to prepare carcinoma cell and hepatocyte suspensions by collagenase digestion. For assay of α2, 3 and α2, 6-sialic acids, the cells were suspended in the staining buffer containing either fluorescein isothiocyanate-Maackia amurensis lectin (FITC-MAL) or fluorescein isothiocyanate-Sambucus nigra bark lectin (FITC-SNA) and incubated for 1 h, respectively. Flow cytometric analysis was carried out to measure the mean fluorescence intensity (MFI) on the cell surface.

RESULTSIn both FITC-MAL- and FITC-SNA-incubated HCC cells, the MFI on the cell surface was greater than that of the hepatocytes.

CONCLUSIONBoth of α2, 3 and α2, 6- sialic acids increases significantly on the hepatocyte membrane after the carcinomatous change.

Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Membrane ; metabolism ; Humans ; Liver Cirrhosis ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Sialic Acids ; metabolism

OBJECTIVETo investigate the expression of cell surface E-cadherin in leukemia cell and the correlation of cell membrane localization of beta-catenin with E-cadherin expression.

METHODSBone marrow samples from 46 patients with acute leukemia and 17 normal donors were analyzed. Cell surface expression of E-cadherin and membrane localization of beta-catenin were labeled by immunofluorescence and analyzed with a laser scanning confocal fluorescence microscope in 14 specimens.

RESULTSCell surface E-cadherin expression level was significantly lower in leukemia cells (with the median fluorescent intensity of 16.78) than in normal hematopoietic progenitors (26.03). Correlation analysis showed that cell membrane localization of beta-catenin was correlated with E-cadherin expression (r = 0.74, P = 0.002). After E-cadherin was induced to express in leukemic cell by 5-Aza-CdR, membranous expression of beta-catenin was elevated while the nuclear expression reduced, indicating that E-cadherin-mediated adhesions could recruit beta-catenin to cell membrane.

CONCLUSIONThe loss of E-cadherin in leukemia cells may result in beta-catenin translocating to the nuclear and transcriptional activation of its target genes.

Cadherins ; metabolism ; Case-Control Studies ; Cell Membrane ; metabolism ; Humans ; Leukemia ; metabolism ; pathology ; beta Catenin ; metabolism

Research on peripheral nervous injuries, especially the stretched injuries, is important to improve the clinical effectiveness and alleviate the patients's pain. In recent years, the biological changes and mechanics of stretched axons have been hot topics. This article reviews the recent advances in the morphological changes of axons as well as changes in cellular membrane, cytoskeleton, cellular metabolism, and action potential after axonal stretch.
Action Potentials ; Animals ; Axons ; metabolism ; pathology ; Cell Membrane ; pathology ; Cytoskeleton ; pathology ; Humans ; Stress, Mechanical

OBJECTIVETo investigate the expression of Podoplanin in lesional epithelia of oral leukoplakia and squamous cell carcinoma and its correlation with lymph vessels density.

METHODSThe expression of Podoplanin in 40 cases of oral leukoplakia, 27 cases of early stage of squamous cell carcinoma and 32 cases of infiltrated stage of squamous cell carcinoma was examined by immunohistochemistry. Meanwhile, the correlation between podoplanin expression in lesional epithelia and its corresponding lymph vessels density was also analysed.

RESULTSPodoplanin expression in epithelia was increased with the exacerbated epithelial proliferation. High expression of Podoplanin in lesional epithelia accounted for 45% in oral leukoplakia, 81% and 78% in early and infiltrated stage of squamous cell carcinoma respectively. Moreover, the lymph vessels density was also increased with the enhanced expression of Podoplanin in oral leukoplakia and early stage of squamous cell carcinoma (P < 0.05). Podoplanin expression in infiltrated stage of squamous cell carcinoma was positively correlated with the lymph vessels density (P < 0.05).

CONCLUSIONSPodoplanin expression in different proliferative oral epithelia may be related to oral carcinogenesis, invasion and metastasis.

Aged ; Biomarkers ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Leukoplakia, Oral ; metabolism ; pathology ; Lymphatic Metastasis ; Lymphatic Vessels ; pathology ; Membrane Glycoproteins ; metabolism ; Mouth Neoplasms ; metabolism ; pathology

Animals ; Arthritis, Experimental ; metabolism ; pathology ; Breast Neoplasms ; pathology ; Cadherins ; metabolism ; physiology ; Cell Movement ; Female ; Fibroblasts ; cytology ; pathology ; Humans ; Macrophages ; cytology ; pathology ; Neoplasm Invasiveness ; Synovial Membrane ; cytology ; metabolism ; pathology

OBJECTIVETo investigate the opening of the mitochondrial permeability transition pores of the cultured hepatocytes in a non-alcoholic fatty liver disease model and its relationship with apoptosis of the cells.

METHODSOleic acid was used to induce cultured L02 hepatocyte steatotic in making a model of NAFLD. The steatotic hepatocytes were detected with oil red O staining; the opening of the mitochondrial permeability transition pores was observed under a fluorescence microscope. The apoptosis of the cells was detected with a flow cytometer.

RESULTSAfter adding oleic acid to the cultured hepatocytes, a model of steatosis of human hepatocytes was established after 24 hours. Oleic acid opened the mitochondrial permeability transition pores of the L02 hepatocytes (72.58%+/-2.78%) more than that in the control group (8.28%+/-4.98%) and the difference was statistically significant (P < 0.01). Apoptosis index of the steatotic hepatocytes at 24 hours and 48 hours were 11.09%+/-4.95% and 15.24%+/-2.45%. They were also higher than those of the control group (4.56%+/-1.25%) (P < 0.05, P < 0.01).

CONCLUSIONOpening the mitochondrial permeability transition pores may be the basis of the apoptosis of steatotic hepatocytes in vitro, and it also may be related to the steatosis of NAFLD in human beings.

Apoptosis ; Cell Line ; Fatty Liver ; metabolism ; pathology ; Hepatocytes ; metabolism ; Humans ; Mitochondria, Liver ; metabolism ; Mitochondrial Membrane Transport Proteins ; metabolism

OBJECTIVETo detect the cell-surface-expressed nucleolin and investigate its tumor suppressing effect on the growth of hepatocellular carcinoma cells.

METHODSTo detect cell-surface-expressed nucleolin in the hepatocellular carcinoma cells by immunofluorescence and flow cytometry. To down-regulate the nucleolin expression level in hepatocellular carcinoma cells by RNA interference. The tumor-suppressing effect of cell-surface nucleolin on hepatocellular carcinoma cells was assessed by MTT and transwell chamber assays.

RESULTSNucleolin was expressed in the nuclei, cytoplasm and on the cell surface of hepatocellular carcinoma cells. ShRNA markedly decreased the nucleolin expression level in the cytoplasm and on the cell surface (P < 0.01), but the nuclear nucleolin remained unchanged. After downregulation of cell-surface nucleolin, MTT assays showed that the cell growth rate of hepatocellular carcinoma cells in the shRNA interference group was significantly inhibited as compared with that in the control group (P < 0.01). The transwell chamber assay showed that the mean transmembrane cell number in the shRNA interference group was significantly lower than that in the control group.

CONCLUSIONThe results of this study show that downregulation of cell-surface nucleolin expression inhibits the growth of hepatocellular carcinoma cells in vitro.

Carcinoma, Hepatocellular ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cell Membrane ; metabolism ; Cell Movement ; Cell Nucleus ; metabolism ; Cell Proliferation ; Cytoplasm ; metabolism ; Down-Regulation ; Humans ; Liver Neoplasms ; genetics ; metabolism ; pathology ; Phosphoproteins ; metabolism ; RNA Interference ; RNA, Small Interfering ; pharmacology ; RNA-Binding Proteins ; metabolism

OBJECTIVETo investigate the influence of hypoxia induced microtubule damage on the opening of mitochondrial permeable transition pore (MPTP)of cardiac myocytes and on the decrease of respiratory function in rat.

METHODSPrimary cultured myocardial cells from 30 neonatal rats were randomized as normoxic group (A), hypoxia group (B), normoxia with microtubule destabilizing agent group (C, with treatment of 8 micromol/L colchicines for 30 minutes before normoxia), and hypoxia with microtubule stabilizing agent group (D, with treatment of 10 micromol/L taxol for 30 minutes before hypoxia). beta-tubulin immunofluorescence ,the opening of mitochondria permeability transition pore, and the mitochondrial inner membrane potential were detected at 0.5, 1, 3, 6 and 12 post-treatment hours (PTH), and the mitochondrial respiratory function was determined by MTT method. The changes in these indices were also determined in A group at the corresponding time-points.

RESULTSObvious damage of polymerized microtubule, opening of MPTP, mitochondrial inner membrane potential loss and decrease of myocardial respiratory activity were observed in both group B and C at 0.5 PTH, and they became more and more serious afterwards. However, the changes in the above indices in D group were much better than those in B group (P < 0.05 or 0.01), and no difference was found between D (92.8 +/- 4.0)% and C [(100.0 +/- 0.0) %, P > 0.05] groups.

CONCLUSIONHypoxia played a role in the myocardial microtubule damage as well as in the opening of MPTP. Moreover, hypoxia could also impair the mitochondrial respiratory function. Microtubule destabilizing agent could reproduce well the process of hypoxia induced microtubule damage, while the stabilizing agent exerted protective effect by improving the transition of mitochondrial permeability and the mitochondria respiratory function.

Animals ; Cell Hypoxia ; Cells, Cultured ; Hypoxia ; metabolism ; pathology ; Membrane Potential, Mitochondrial ; Microtubules ; pathology ; Mitochondria, Heart ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo detect the expression of macrophage inflammatory protein-1alpha (MIP-1alpha), a disintegrin-like and metalloproteinase (ADAM) 8 and 12 and CD68 protein in giant cell lesions of jaw and giant cell tumors of long bone, and to study their effects on the histogenesis of giant cells in such lesions.

METHODSMIP-1alpha, ADAM8, ADAM12 and CD68 were detected by immunohistochemistry in 24 paraffin-embedded specimens of central giant cell lesions of jaw and giant cell tumors respectively.

RESULTSMIP-1alpha positive signal was located in blood vessels and bone. ADAM8, ADAM12 and CD68 positive signals were located in the cell membrane and cytoplasm of all multinucleated giant cells and some round mononuclear cells in the lesions. In addition, some spindle mononuclear stromal cells were positive for ADAM12 in both lesions.

CONCLUSIONMultinucleated giant cells probably originate from CD68-postive round mononuclear cells, which are recruited from monocyte-macrophage system by chemokines, such as MIP-1alpha, followed by cell fusion mediated by ADAM8 and ADAM12.

ADAM Proteins ; metabolism ; ADAM12 Protein ; Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Bone Neoplasms ; metabolism ; pathology ; Cell Membrane ; metabolism ; Chemokine CCL3 ; Chemokine CCL4 ; Cytoplasm ; metabolism ; Giant Cell Tumor of Bone ; metabolism ; pathology ; Giant Cells ; metabolism ; Granuloma, Giant Cell ; metabolism ; pathology ; Humans ; Jaw Diseases ; metabolism ; pathology ; Macrophage Inflammatory Proteins ; metabolism ; Membrane Proteins ; metabolism