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At least 199 records · Page 11Linked to original sources
PubMed2006

Sphingosine 1-phosphate as a regulator of osteoclast differentiation and osteoclast-osteoblast coupling.

Sphingosine 1-phosphate (S1P), produced by sphingosine kinase (SPHK), acts both by intracellular and extracellular modes. We evaluated the role of SPHK1 and S1P in osteoclastogenesis using bone marrow-derived macrophage (BMM) single and BMM/osteoblast coculture systems. In BMM single cultures, the osteoclastogenic factor receptor activator of NF-kappaB ligand (RANKL) upregulated SPHK1 and increased S1P production and secretion. SPHK1 siRNA enhanced and SPHK1 overexpression attenuated osteoclastogenesis via modulation of p38 and ERK activities, and NFATc1 and c-Fos levels. Extracellular S1P had no effect in these cultures. These data suggest that intracellular S1P produced in response to RANKL forms a negative feedback loop in BMM single cultures. In contrast, S1P addition to BMM/osteoblast cocultures greatly increased osteoclastogenesis by increasing RANKL in osteoblasts via cyclooxygenase-2 and PGE(2) regulation. S1P also stimulated osteoblast migration and survival. The RANKL elevation and chemotactic effects were also observed with T cells. These results indicate that secreted S1P attracts and acts on osteoblasts and T cells to augment osteoclastogenesis. Taken together, S1P plays an important role in osteoclastogenesis regulation and in communication between osteoclasts and osteoblasts or T cells.

Animals↗
PubMed2004

In situ localization of mRNA for the fibrinolytic factors uPA, PAI-1 and uPAR in endometriotic and endometrial tissue.

Endometriotic tissue grows invasively. The plasminogen-activating system is suggested to participate in degradation of extracellular matrix (ECM) and modulation of cell adhesion and migration. We have previously demonstrated elevated levels of the fibrinolytic factors urokinase plasminogen activator (uPA) and plasminogen activator inhibitor (PAI-1) in endometriotic tissue and endometrium from women with endometriosis. The aim of the present study was to localize the uPA, PAI-1 and urokinase plasminogen activator receptor (uPAR) mRNA in endometriotic tissue and in endometrium both from women with and without endometriosis. With in situ hybridization, we found that uPA mRNA seems to be up-regulated in endometriotic glands and endometrial stroma as well as PAI-1 mRNA in endometriotic and endometrial stroma from women with endometriosis. uPAR mRNA likewise appears to be up-regulated in both glands and stroma in endometriotic tissue and in endometrial glands from patients compared to endometrial glands and stroma from healthy women. These differences might be important for menstrual shedding and adherence of endometrial fragments to peritoneal lining in women developing endometriosis and for the invasive growth of endometriotic tissue.

Endometriosis↗
PubMedDate not supplied

Genetic susceptibility and resistance to diet-induced atherosclerosis and hyperlipoproteinemia.

To test the hypothesis that genetic susceptibility or resistance to diet-induced atherosclerosis is correlated with serum levels of specific lipids, lipoproteins, or apoproteins, male mice of a genetically susceptible and a genetically resistant strain were fed either a normal or an atherogenic diet. After 20 weeks on a normal diet, neither the resistant nor the susceptible strain mice had atherosclerosis; resistant strain mice had serum cholesterol of 66 +/- 11 while the susceptible strain mice had 90 +/- 1 mg/dl serum cholesterol, and lipoproteins were dominated by a single alpha-migrating HDL. After 20 weeks on an atherogenic diet, resistant strain mice had 185 +/- 55 mg/dl cholesterol, their lipoproteins remained dominated by alpha-migrating HDL, and two of eight mice had mild atherosclerotic lesions; susceptible strain mice had 510 +/- 94 mg/dl cholesterol, multiple alpha- and pre-beta-migrating lipoprotein species, and all 13 had advanced aortic atherosclerosis. The resistant strain mice had an apolipoprotein E/total lipoprotein protein ratio of 0.42 on the normal diet and 0.53 on the atherogenic diet, while the susceptible strain mice had the significantly lower ratios of 0.07 and 0.31, respectively. These data indicate that genetic resistance to diet-induced aortic atherosclerosis in mice is correlated with capacity to prevent large increases in serum cholesterol, to suppress abnormal alpha- and pre-beta-migrating lipoproteins, and to maintain elevated serum apolipoprotein E/total lipoprotein protein ratios. Our data do not preclude the possibility of additional gene control at the level of arterial end organ response.

Animals↗
PubMed1984

Neutrophil migration through test end tissues of bovine mammary quarters experimentally challenged with Staphylococcus aureus.

Diapedesis and infiltration of neutrophils into internal epithelial tissues of the distal teat end and migration into milk were studied in bovine mammary quarters infected with Staphylococcus aureus. Neutrophil extravasation, penetration of the epithelium, and mode of passage into milk were evaluated by light and transmission electron microscopy. Collection of observations from 10 infected quarters of six cows provided morphologic evidence for the following sequence of events as neutrophils passed from blood into milk. In capillaries of the subepithelial stroma, neutrophils adhered to luminal walls, penetrated endothelia and basal lamina, then migrated across the periendothelial cell layer into extravascular connective tissues adjacent to epithelial linings. The leukocytes then penetrated epithelial basal laminae and migrated between basal epithelial cells to gain access to the luminal cell layer. Possible modes of migration across luminal cells into milk included 1) projection through individual, degenerate luminal cells, 2) penetration between intact epithelia, and 3) passage into milk as luminal cells desquamated in areas of epithelial metaplasia. The first method appeared to be the predominant mechanism of migration. These data suggest that elevated numbers of neutrophils in distal teat end epithelium and in cisternal milk may be instrumental in the initial events that prevent establishment of infection in the bovine mammary gland.

Animals↗
PubMed2002

Regulation of macrophage-derived chemokine (MDC, CCL22) production.

Macrophage-derived chemokine (MDC, CCL22) is a member of the CC-chemokine family and is composed of 69 amino acid residues. MDC is mainly produced by macrophages and dendritic cells upon the stimulation with microbial products, or anti-CD40 antibody, and is upregulated by TH2-type cytokines, such as IL-4 and -5, but is downregulated by TH1-type cytokines, such as IFN-gamma. MDC-production is also upregulated by prostaglandin and cyclic AMP-elevating agents. MDC causes chemotactic migration of dendritic cells and TH2 cells. Furthermore, MDC is highly-expressed in the lesions of TH2-related diseases, such as airway hypersensitivity and atopic dermatitis. Thus, MDC plays an important role in the recruitment of TH2 cells into the inflammatory sites and the regulation of TH2-related immune responses.

Animals↗
PubMed1999

Effects of 16O+6 ion irradiation on human sperm spontaneous chemiluminescence, motility, acrosome reaction and viability in vitro.

Effects of 16O+6 ion irradiation with different doses on human sperm spontaneous chemiluminescence (SCL), motility, acrosome reaction (AR) and viability were examined. Spermatozoa were irradiated with 0, 0.25, 0.5, 1, 2, 4, 8, 16, 32, or 64 Gy 16O+6 ion beam at the energy of 3.17 MeV/u. After irradiation, samples were analyzed by SCL measurement at 1, 2 and 3 h of incubation; motility was determined by the transmembrane migration method within 2 h of incubation; the percentage of AR and viability was evaluated by the triple-stain technique at 3.5 h of incubation. The results showed: sperm SCL was significantly increased with irradiation doses and the lowest effective dose was 0.5 Gy; compared with controls, the transmembrane migration ratio of spermatozoa progressively elevated with irradiation doses at 0.5, 1, and 2 Gy; the percentage of sperm AR markedly increased in 0.5-4 Gy irradiation and the optimal dose was 2 Gy, and then significant decreased with further increase of irradiation doses; the viability had no significant change within 0.25-8 Gy, but was progressively decreased at 16, 32 and 64 Gy. These data suggested that heavy ion at low doses increased motility and AR, whereas had deleterious effects at higher doses, which are associated with free radical reactions induced by heavy ion irradiation.

Acrosome Reaction↗
PubMed2006

Arthroscopic approach to massive rotator cuff tears.

The treatment of a patient with a painful massive rotator cuff tear can be challenging. Massive tears exceed 5 cm in length and involve partial or complete tearing of three tendons. The arthroscopic approach provides a minimally invasive technique to evaluate the tear, mobilize and repair tendons, and improve symptoms without disruption of the deltoid. The arthroscopic technique can create a low-tension repair. The reduction of postoperative motion provides the best environment for tendon-to-bone reattachment. Procedures that have reduced rates of adhesion formation allow for this protection with a minimal risk of stiffness. Reduction of the boutonniere effect of superior head migration leads to improved arm elevation. Strength deficits are common and relate to muscle and tendon deterioration that may not be reversible, even with successful closure of the tear. Weakness caused by suprascapular neuropathy may improve after the position and length of the posterosuperior cuff tendons are reestablished. Arthroscopic options include rotator cuff repair, partial cuff repairs, xenografts, decompression, débridement, biceps tenotomy, tenodesis, and use in autografting.

Arthroscopy↗
PubMed1984

[Studies on changes of lysozyme activity during pre- and postoperative periods in alimentary tract surgery].

From the clinical and experimental studies, the following results were obtained. The serum lysozyme activity decreased postoperatively and returned to the preoperative level 2 weeks later. Postoperative changes of the activity reflected the state of surgical stress inflicted on the subjects, namely, the changes were parallel to the degree of the stress and their postoperative courses. The postoperative elevation of lysozyme activity in anastomosed colonic tissues or abdominal walls, in which the activity was not determined preoperatively was supposed to be a reasonable phenomenon and closely related to tissue regeneration or protection from bacterial infection. The mechanism of this local elevation should be due to migration from the peripheral blood and movement of the lysozyme-producing or -secreting cells to the wounds. The phagocytic activity of peritoneal macrophage hyperfunctioned postoperatively. This might suggest lysozyme synthesis or secretion by peritoneal macrophage and participate in the protective action of the subjects. The postoperative serum lysozyme activity was maintained at the normal level by preoperative peroral administration of egg-white lysozyme preparation, therefore, the administration was thought to be very effective to the acceleration of protective action of the subjects on whom the surgical stress was imposed.

Aged↗
PubMed1997

In-situ endothelial cell adhesion molecule expression in ulcerative colitis. E-selectin in-situ expression correlates with clinical, endoscopic and histological activity and outcome.

BACKGROUND AND OBJECTIVES: Little is known of the in-situ expression of adhesion molecules in ulcerative colitis (UC) according to disease activity. In the present study we investigate the vascular expression of endothelial leucocyte adhesion molecule 1 (ELAM-1/E-selectin), vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecules (ICAM-1 and ICAM-3) on the rectal mucosa of patients with UC in order to identify links between in-situ expression of these adhesion molecules and clinical, endoscopic and histological parameters. DESIGN AND METHODS: At inclusion, 16 untreated patients with UC at different stages of disease activity were assessed clinically and endoscopically and underwent rectal biopsy. Ten patients had similar assessments during follow-up. Quantitative histological and immunohistochemical scores were established with anti-E-selectin, VCAM-1, ICAM-1, ICAM-3 and HLA-DR monoclonal antibodies on frozen biopsy specimens. RESULTS: (1) At inclusion, E-selectin in-situ expression correlated with clinical activity (r = 0.7, P = 0.05), endoscopic severity (r = 0.74, P = 0.04), the histological score (r = 0.57, P = 0.02) and in-situ expression of HLA-DR on epithelial cells (r = 0.74, P = 0.01). (2) After remission, there was a significant decrease in ELAM-1 in-situ expression (P = 0.04). (3) In patients with clinical, endoscopic and histological remission the level of residual E-selectin expression appeared to be predictive of clinical relapse. (4) Vascular expression of VCAM-1 and ICAM-1 did not correlate with clinical, endoscopic or histological parameters, or with changes in disease activity. (5) ICAM-3 was never detected on endothelial cells of the colonic mucosa of controls or patients with UC. CONCLUSION: In ulcerative colitis, E-selectin, but not VCAM-1, ICAM-1 or ICAM-3, appears to play a central role in leucocyte migration into the colonic mucosa. Elevated vascular expression of E-selectin after remission may be involved in clinical recurrence.

Adult↗
PubMed1976

Immunodeficiencies in severe atopic dermatitis. Depressed chemotaxis and lymphocyte transformation.

Various reports have indicated assorted immune defects in atopic dermatitis, but the prevalence and degree of the defects remain unclear. We assessed various immunological factors in 14 patients with atopic dermatitis to determine whether immunodeficiencies were present consistently and were reflected by the patients' clinical characteristics. A high incidence of cutaneous infection was noted. Cutaneous delayed-hypersensitivity testing showed anergy in eight (67%) patients. Only the seven patients with the most severe condition showed altered leukocyte function, as determined by polymorphonuclear and mononuclear leukocyte chemotaxis and by lymphocyte responsiveness to phytohemaglutinin. All three cell types where shown to be simultaneously dysfunctional during severe atopic flares. Chemotactic studies during clinical remissions disclosed notable improvement in cell migration. Serum IgE levels were elevated in each patient, but did not correlate with the degree of cutaneous anergy or altered leukocyte function.

Adult↗
PubMed2000

Muscarinic activation of BK channels induces membrane oscillations in glioma cells and leads to inhibition of cell migration.

Patients with cerebral tumors often present with elevated levels of acetylcholine (ACh) in their cerebrospinal fluid. This motivated us to investigate physiological effects of ACh on cultured human astrocytoma cells (U373) using a combination of videomicroscopy, calcium microspectrofluorimetry and perforated patch-clamp recording. Astrocytoma cells exhibited the typical morphological changes associated with cell migration; polarized cells displayed prominent lamellipodia and associated membrane ruffling at the anterior of the cell, and a long tail region that periodically contracted into the cell body as the cell moved forward. Bath application of the ACh receptor agonist, muscarine, reversibly inhibited cell migration. In conjunction with this inhibition, ACh induced a dose-dependent, biphasic increase in resting intracellular free calcium concentration ([Ca2+]i) associated with periodic Ca2+ oscillations during prolonged ACh applications. The early transient rise in [Ca2+]i was abolished by ionomycin and thapsigargin but was insensitive to caffeine and ryanodine while the plateau phase was strictly dependent on external calcium. The Ca2+ response to ACh was mimicked by muscarine and abolished by the muscarinic antagonists, atropine or 4-DAMP, but not by pirenzepine. Using perforated patch-clamp recordings combined with fluorescent imaging, we demonstrated that ACh-induced [Ca2+]i oscillations triggered membrane voltage oscillations that were due to the activation of voltage-dependent, Ca2+-sensitive K+ currents. These K+ currents were blocked by intracellular injection of EGTA, or by extracellular application of TEA, quinine, or charybdotoxin, but not by apamin. These studies suggest that activation of muscarinic receptors on glioma cells induce the release of Ca2+ from intracellular stores which in turn activate Ca2+-dependent (BK-type) K+ channels. Furthermore, this effect was associated with inhibition of cell migration, suggesting an interaction of this pathway with glioma cell migration.

Acetylcholine↗
PubMed2003

Cyclic AMP inhibits production of interleukin-6 and migration in human vascular smooth muscle cells.

BACKGROUND: Gene expression induced by tumor necrosis factor-alpha (TNF-alpha) is involved in the regulation of vascular smooth muscle cell (VSMC) proliferation and migration, two events critical to formation of stenotic vascular lesions. In some systems, elevating adenosine 3',5'-cyclic monophosphate (cyclic AMP) inhibits TNF-alpha induced gene transcription. We recently demonstrated that interleukin-6 (IL-6) was chemotactic to VSMC. Therefore, we tested the hypothesis that elevating cyclic AMP would inhibit TNF-alpha-mediated IL-6 expression and VSMC migration. MATERIALS AND METHODS: VSMC were cultured from saphenous vein remaining after coronary artery bypass grafting. Migration of VSMC through a porous membrane was determined. Intracellular cyclic AMP was elevated by exposing the cells to forskolin or 8-Br-cyclic AMP and was measured by radioimmunoassay. IL-6 was measured by enzyme-linked immunosorbent assay. RESULTS: TNF-alpha induced migration of VSMC in a concentration-dependent manner. Incubation of cells with forskolin significantly increased cyclic AMP. Co-incubation of cells with TNF-alpha in combination with 8-Br-cyclic AMP or forskolin inhibited migration by approximately 25 and 70%, respectively. Incubation with TNF-alpha increased release of IL-6 from VSMC 18-fold over basal. This stimulated release was inhibited by either 8-Br-cyclic AMP or forskolin. In cells stimulated with TNF-alpha, addition of an antibody to IL-6 reduced migration by 25%. CONCLUSIONS: These data show that IL-6 produced by VSMC contributes to cell migration induced by TNF-alpha. Further, elevating cyclic AMP inhibited TNF-alpha-induced release of IL-6, and migration of VSMC. These results are consistent with the notion that mechanisms that increase intracellular cyclic AMP, such as activation of beta-adrenergic receptors on VSMC, act as a brake on cell migration.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2006

Attractin is elevated in the cerebrospinal fluid of patients with malignant astrocytoma and mediates glioma cell migration.

PURPOSE: There are a limited number of noninvasive methods available for the monitoring of neoplastic disease in the central nervous system. The goal of our study was to find reliable markers that could be used for disease monitoring as well as to identify new targets for the therapeutic intervention for malignant astrocytoma (WHO grades 3 and 4). EXPERIMENTAL DESIGN: We employed proteomic techniques to identify secreted proteins in the cerebrospinal fluid that were specific to patients with malignant astrocytoma. RESULTS: Among 60 cerebrospinal fluid samples of patients with various central nervous system diseases, attractin was consistently found to be elevated in the samples of patients with malignant astrocytoma. To independently validate these results, we examined attractin expression in a new set of 108 normal and tumoral brain tissue specimens and found elevated expression in 97% of malignant astrocytomas, with the highest levels in grade 4 tumors. Using immunohistochemistry, we further showed that attractin is produced and secreted by the tumor cells. Finally, we showed that cerebrospinal fluid from brain tumor patients induces glioma cell migration and that attractin is largely responsible for this promigratory activity. CONCLUSIONS: Our results find attractin to be a reliable secreted marker for high-grade gliomas. Additionally, our migration studies suggest that it may be an important mediator of tumor invasiveness, and thus, a potential target in future therapies.

Astrocytoma↗
PubMed2002

Phospholipase D2 stimulates cell protrusion in v-Src-transformed cells.

Phospholipase D (PLD) activity has been implicated in several aspects of cell physiology including vesicle transport, signal transduction, cell proliferation, cytoskeletal structure, and oncogenic transformation. Two PLD isoforms (PLD1 and PLD2) have been identified and characterized. We have expressed both wild-type and catalytically inactive forms of PLD1 and PLD2 in 3Y1 rat fibroblasts and in 3Y1 cells transformed by v-Src, a tyrosine kinase that elevates PLD activity. The v-Src-transformed 3Y1 cells have small, but distinct cell protrusions, implicated in cell migration and metastasis. We report here that elevated expression of PLD2 substantially increased the length of the cell protrusions and that a catalytically inactive PLD2 mutant abolished the cell protrusions. The extended protrusions in the PLD2-overexpressing cells were dependent upon microtubule assembly. These data suggest a role for PLD2 in the v-Src-mediated formation of cell protrusions that may be critical for the invasive properties of v-Src-transformed cells.

Animals↗
PubMedDate not supplied

Antiproliferative and antimigratory effects of doxorubicin in human osteosarcoma cells exposed to extracellular matrix.

Osteosarcoma cells are involved in the remodeling of the extracellular matrix (ECM) that affects their growth, invasive and metastatic activities. The tumour ECM provided effective protection against chemotherapy agents in several previously studied malignancies. The current study examined the effects of doxorubicin on cells that were migrated into a 3-dimensional extracellular matrix gel (ECM-gel) in comparison with its effects on cells remaining in the monolayer compartment. A human osteosarcoma cell line (OSCORT) was treated with doxorubicin in monolayer culture for 4 or 24 hours, and then overlaid by ECM-gel for 24 hours. Tumour cells remaining in the monolayer were separated from the cells migrated into ECM-gel, and both of them were characterized. OSCORT cells migrated into ECM-gel showed elevated levels and activity of topoisomerase II, increased protein expression of beta1 integrin and matrix metalloproteinase-9 activity. Doxorubicin treatment for 4 hours resulted in increased cytotoxicity in the monolayer compartment relative to the cells migrated into ECM-gel, whereas 24-hour treatment at a low concentration (0.01 microg/ml) showed an antimigratory effect. Different antiproliferative and antimigratory effects of doxorubicin treatment schedules warrant short-term, high-dose treatment for targeting the tumour growth, and long-term, low-dose treatment for targeting the invasion of osteosarcoma.

Antibiotics, Antineoplastic↗
PubMed1999

Changes in patterns of corticosterone secretion concurrent with migratory fattening in a neotropical migratory bird.

Several studies on free-living birds have shown a change in corticosterone secretion (elevated baseline levels and a reduced corticosterone response to stress) during migration. It was not known, however, if this change was concurrent with the development of migratory condition or if it was an independent response to unknown environmental stressors experienced by the birds prior to capture. In this study, a Neotropical annual migrant, the yellow-rumped warbler (Dendroica coronata), held under controlled laboratory conditions, was used to test the Migration Modulation Hypothesis (MMH): during the migratory period migrants exhibit (1) elevated baseline corticosterone to facilitate migratory fattening and (2) a reduced corticosterone stress response, a means by which skeletal muscle needed for migration can be protected against catabolism by high levels of corticosterone. Fifteen hatching-year warblers were maintained on insect larvae and water ad libitum for 43 weeks, experiencing two transitions from a short- to long-day photoperiod to bring them into spring migratory condition. Corticosterone profiles comprising three blood samples from each individual (baseline at the time of initial disturbance and 30 and 60 min later), body mass, fat reserves, molt, and state of cloacal protuberance (males only) were measured at key intervals throughout the study. Over the entire study, mean baseline corticosterone levels were positively correlated with mean body mass, which increased predictably in response to long days. Individual baseline corticosterone was not correlated with individual body mass at any time. During periods when the birds were lean and held on short days, the corticosterone stress profiles were characterized by low initial hormone concentration followed by a significant increase in corticosterone with handling time. In response to long days, the warblers showed a significant increase in body mass and fat reserves concurrent with corticosterone stress profiles characterized by significantly elevated baseline levels and no further increase in corticosterone with handling time. These results support both components of the MMH illustrating changes in corticosterone secretion concurrent with migratory fattening but the exact nature of this change is unknown.

Adipose Tissue↗
PubMed1987

Cellular and humoral immune responses in experimental aspergillosis in mice.

Invasive aspergillosis was established in a naive murine model. Both humoral and cellular aspects of the immunological mechanism responded to invasion. Circulating immune complexes containing IgG in the infected group of animals were detected by both the C1q and conglutinin solid phase assays. Attempts to identify these complexes as Aspergillus antigen-specific complexes were unsuccessful. Cellular responses, as measured by blastogenic activity and inhibition of migration of sensitized cells were significantly elevated in the infected group.

Animals↗
PubMed2003

Schizophrenia hippocampus has elevated expression of chondrex glycoprotein gene.

To identify genes associated with schizophrenia, DNA microarray chips were used to compare schizophrenia and control hippocampus tissues, revealing four genes with elevated expression, chondrex (or YKL-40), histamine-releasing factor, HERC2, and heat-shock 70. However, using the quantitative real-time polymerase chain reaction method, only the expression of the chondrex gene, an extracellular matrix glycoprotein involved in cell growth and migration, was found to be significantly elevated, by 1.8-fold. Real-time PCR found that the expression of the histamine-releasing factor gene, known to be associated with cognitive deficits in Alzheimer's disease, was significantly reduced by 19%. The expression of the HERC2 and heat-shock 70 genes, as measured by real-time PCR, were not significantly altered in the schizophrenia hippocampus. The altered gene expression of chondrex suggests that disruption in neuronal migration may be involved in schizophrenia. The change in expression of the histamine-releasing factor gene suggests that this gene may be associated with the negative symptoms of impaired learning and memory in schizophrenia.

Adipokines↗