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PubMed1999

Homocysteine enhances neutrophil-endothelial interactions in both cultured human cells and rats In vivo.

Despite intense investigation, mechanisms linking the development of occlusive vascular disease with elevated levels of homocysteine (HCY) are still unclear. The vascular endothelium plays a key role in regulating thrombogenesis and thrombolysis. We hypothesized that vascular lesions in individuals with elevated plasma HCY may be related to a dysfunction of the endothelium triggered by HCY. We investigated the effect of HCY on human neutrophil adhesion to and migration through endothelial monolayers. We also examined the effect of HCY on leukocyte adhesion and migration in mesenteric venules of anesthetized rats. We found that pathophysiological concentrations of HCY in vitro induce increased adhesion between neutrophils and endothelial cells. This contact results in neutrophil migration across the endothelial layer, with concurrent damage and detachment of endothelial cells. In vivo, HCY infused in anesthetized rats caused parallel effects, increasing leukocyte adhesion to and extravasation from mesenteric venules. Our results suggest that extracellular H2O2, generated by adherent neutrophils and/or endothelial cells, is involved in the in vitro endothelial cell damage. The possibility exists that leukocyte-mediated changes in endothelial integrity and function may lead to the vascular disease seen in individuals with elevated plasma HCY.

Animals↗
PubMed1984

Tumor-promoting phorbol esters stimulate the phosphorylation of ribosomal protein S6 in quiescent Reuber H35 hepatoma cells.

The addition of the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) to serum-starved quiescent Reuber H35 hepatoma cells results in a rapid 5- to 11-fold increase in the incorporation of 32Pi into a Mr = 32,000 ribosomal protein. The Mr = 32,000 protein was the major phosphorylated protein extracted from isolated 80 S ribosomes and was identified as the 40 S ribosomal protein S6 based upon its migration in two-dimensional gels. Insulin, which has been demonstrated to increase the phosphorylation of S6 in a number of cell lines, caused a 10- to 20-fold increase in the incorporation of 32Pi into this Mr = 32,000 ribosomal protein. S6 phosphorylation was dose- and time-dependent being detected as early as 5 min following the addition of 1.6 microM TPA. Maximal phosphorylation of ribosomal protein S6 was achieved by 60 min and remained elevated for at least 90 min in the presence of TPA. The 50% effective dose for TPA was estimated to be 0.14 microM. Based upon the altered migration of S6 in pH 8.5 urea-polyacrylamide gels, it was demonstrated that the increased 32Pi labeling of S6 by TPA was due to a net increase in the incorporation of phosphates into the S6 molecule. Non-tumor-promoting phorbol esters were ineffective in increasing the phosphorylation of S6. In whole cells, exogenously added 1 mM 8-bromoadenosine 3':5'-monophosphate failed to substantially increase phosphorylation of S6 suggesting that the TPA-induced phosphorylation of S6 occurs via a cyclic AMP-independent mechanism. The S6 amino acid residue phosphorylated in response to TPA was phosphoserine. A possible role for protein kinase C in the phosphorylation of ribosomal protein S6 is discussed.

Animals↗
PubMed1994

Soluble intercellular adhesion molecule-1 in primary biliary cirrhosis: relationship with disease stage, immune activity and cholestasis.

Intercellular adhesion molecule-1, strongly expressed on the interlobular and proliferating bile ducts in primary biliary cirrhosis, is important in the migration and adhesion of inflammatory cells from the circulation to these structures. A soluble form has been found to be elevated in serum in primary biliary cirrhosis. Our aim was to check on the role of soluble intercellular adhesion molecule-1 in primary biliary cirrhosis with particular reference to its specificity by comparison with other disease control groups and to assess its relationship with stage of disease activity, circulating lymphocyte activation and cholestasis. Soluble intercellular adhesion molecule-1 (enzyme-linked immunosorbent assay) and liver biochemistry were measured in 41 patients with primary biliary cirrhosis, 9 with primary sclerosing cholangitis, 12 with alcoholic liver disease and 17 healthy controls. In subgroups of patients with primary biliary cirrhosis, lymphocyte activation and hepatic bile acid uptake and excretory rates were determined. Soluble intercellular adhesion molecule-1 was significantly higher in all three disease groups. Levels in primary biliary cirrhosis and primary sclerosing cholangitis were similar and significantly higher than alcoholic liver disease. Soluble intercellular adhesion molecule-1 expression was greater in late primary biliary cirrhosis than early disease and correlated with histological progression. Correlations were also found with alkaline phosphatase, gamma-glutamyl transpeptidase and conjugated bilirubin. A trend toward an inverse correlation with hepatic excretory rate was found, but no correlation was detected with circulating lymphocyte interleukin-2 receptor expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Accumulation profiles of persistent organochlorines in waterbirds from an estuary in Korea.

Persistent organochlorine pollutants (POPs), such as polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and organochlorine (OC) pesticides such as DDTs (dichlorodiphenyltrichloroethane), HCHs (hexachlorocyclohexane isomers), CHLs (chlordane compounds) and HCB (hexachlorobenzene), were measured in subcutaneous fat of resident and migratory birds collected from the Nakdong River estuary (NRE) in Korea. Black-tailed gull, a resident bird from the NRE, contained greater concentrations of PCDD/Fs and PCBs than the migratory birds collected in the estuary. For example, mean concentrations of PCDD/Fs in black-tailed gull (395.5 pg/g fat weight) were higher than those in migratory birds, such as greenshank (198.3 pg/g fat weight), common gull (90.9 pg/g fat weight) black-headed gull (84.2 pg/g fat weight), and common tern (47.1 pg/g fat weight). However, concentrations of DDTs and/or HCHs were great in some migratory species, such as little tern (mean DDT 6,200 ng/g fat weight) and black-necked grebe (HCHs 475 ng/g fat weight). This suggested that contamination of PCDD/Fs and PCBs in resident gulls are due to intake of locally contaminated fish near the NRE. Elevated OC pesticide levels in migratory birds indicated that these birds have been exposed to DDTs and HCHs during their migration in Southeast Asian countries where chlorinated pesticides are still used. 2,3,7,8-Tetrachloro dibenzo-p-dioxin equivalents (TEQs) were calculated using the toxic equivalency factors (TEFs) reported by World Health Organization in 1998. Four of the 2,3,7,8-substituted congeners of PCDD/Fs contributed over 90% of the TEQs.

Adipose Tissue↗
PubMed1984

The Papillon-Lefèvre syndrome: neutrophil dysfunction with severe periodontal disease.

Two cases of Papillon-LeF evre are described. Both siblings demonstrated neutrophil dysfunction and severe precocious periodontal disease. The neutrophil locomotion defect was characterized by a decreased migration toward a chemotactic factor and decreased random migration. Binding of the chemotactic factor, FMLP, to the neutrophil surface was unchanged. Both patients harbored Actinobacillus actinomycetemcomitans and showed elevated serum IgG levels. Both patients also demonstrated salivary and serum antibody to A. actinomycetemcomitans. The Papillon-LeF evre syndrome is compared with the more common localized juvenile periodontitis.

Actinobacillus↗
PubMed2006

Salinity effects on activity and expression of glutathione S-transferases in white sturgeon and Chinook salmon.

This study evaluated the activity and expression of the glutathione S-transferase (GST) detoxification isoenzymes in juvenile white sturgeon (Acipenser transmontanus) and Chinook salmon (Oncorhynchus tshawytscha) during acclimation from freshwater (2 per thousand) to estuarine (15 per thousand) salinity conditions. In white sturgeon, GST activity toward 1-chloro-2,4-dinitrobenzene (CDNB) increased significantly (P = 0.005; n = 5) with elevated salinity, but not for the Chinook salmon (P = 0.174; n = 10). GST activity of both sturgeon and salmon toward ethacrynic acid (ETHA) did not significantly change with elevated salinity (P = 0.516 with n = 3, and P = 0.125 with n = 3, respectively). Expression of the GST classes, and hepatic glutathione (GSH) concentration, as determined by HPLC, also did not significantly change with increased salinity. In conclusion, overall GST activity in white sturgeon, but not Chinook salmon, is stimulated by elevated water salinity, thus electrophilic chemicals such as pesticides may be more effectively detoxified by sturgeon as they undergo seaward migration.

Animals↗
PubMed2006

Pathological muscle activation patterns in patients with massive rotator cuff tears, with and without subacromial anaesthetics.

A mechanical deficit due to a massive rotator cuff tear is generally concurrent to a pain-induced decrease of maximum arm elevation and peak elevation torque. The purpose of this study was to measure shoulder muscle coordination in patients with massive cuff tears, including the effect of subacromial pain suppression. Ten patients, with MRI-proven cuff tears, performed an isometric force task in which they were asked to exert a force in 24 equidistant intervals in a plane perpendicular to the humerus. By means of bi-polar surface electromyography (EMG) the direction of the maximal muscle activation or principal action of six muscles, as well as the external force, were identified prior to, and after subacromial pain suppression. Subacromial lidocaine injection led to a significant reduction of pain and a significant increase in exerted arm force. Prior to the pain suppression, we observed an activation pattern of the arm adductors (pectoralis major pars clavicularis and/or latissimus dorsi and/or teres major) during abduction force delivery in eight patients. In these eight patients, adductor activation was different from the normal adductor activation pattern. Five out of these eight restored this aberrant activity (partly) in one or more adductor muscles after subacromial lidocaine injection. Absence of glenoid directed forces of the supraspinate muscle and compensation for the lost supraspinate abduction torque by the deltoideus leads to destabilizating forces in the glenohumeral joint, with subsequent upward translation of the humeral head and pain. In order to reduce the superior translation force, arm adductors will be co-activated at the cost of arm force and abduction torque. Pain seems to be the key factor in this (avoidance) mechanism, explaining the observed limitations in arm force and limitations in maximum arm elevation in patients suffering subacromial pathologies. Masking this pain may further deteriorate the subacromial tissues as a result of proximal migration of the humeral head and subsequent impingement of subacromial tissues.

Aged↗
PubMed1985

Ovine hydatidosis: some immunological characteristics of the seronegative host.

The immune status of a group of sheep naturally infected with hydatid cysts was investigated. Low specific anti-hydatid antibody (Sab) titres and negative results in intradermal and leucocyte migration tests occurred in hosts with high hydatid antigen-stimulated lymphocyte transformation (LT). Total (non-specific) IgG was elevated in infected sheep and was positively correlated with LT. Circulating hydatid antigen (cAg) was detectable in some infected sheep, but not in all of those with low Sab. Relationships between cAg, Sab and immune complex levels suggest that most cAg is present in immune complexes.

Animals↗
PubMed2002

Macrophage inflammatory protein 3alpha-CC chemokine receptor 6 interactions play an important role in CD4+ T-cell accumulation in periodontal diseased tissue.

The regulatory role of chemokines and chemokine receptors on specific lymphocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that lymphocytes infiltrating inflamed gingival tissue expressed marked levels of CCR6. In periodontal diseased tissue, the expression of MIP-3alpha mRNA was detected by RT-PCR and further, MIP-3alpha was distributed in the basal layer of gingival epithelial cells, microvascular endothelial cells and the areas of inflammatory cells as shown by immunohistochemistry. Moreover, CCR6-expressing cells infiltrated into periodontal diseased tissue, and the proportion of CCR6-positive CD4+ T cells was significantly elevated in periodontal diseased tissue compared with peripheral blood in the same patients. Furthermore, gingival lymphocytes isolated from patients showed migration toward MIP-3alpha in an in vitro chemotaxis assay in which migration was abrogated by specific antibody to CCR6. Thus, these findings suggested that CCR6 and the corresponding chemokine, MIP-3alpha may have an important regulatory role in specific lymphocyte migration into inflamed periodontal tissue.

Adult↗
PubMed2002

Mechanisms of 5-azacytidine (5AzC)-induced toxicity in the rat foetal brain.

Mechanisms of 5-azacytidine (5AzC)-induced toxicity in the rat foetal brain were investigated. 5AzC (10 mg/kg) was injected into pregnant rats on day 13 of gestation and the protein and mRNA expressions of p53 and its transcriptional target genes, p21, bax, cyclin G1, fas, and gadd45, were examined in the foetal brain. The number of p53-positive cells peaked at 9 h after treatment (HAT) and those of apoptotic cells and p21-positive cells peaked at 12 HAT. The expressions of p21, bax, cyclin G1, and fas mRNAs were significantly elevated from 9 to 12 HAT. From the experiments using 5-bromo-2'-deoxyuridine (BrdU), as compared with controls, the migration of neuroepithelial cells significantly delayed and BrdU-positive signals were observed in many apoptotic cells from 9 to 24 HAT in the 5AzC-group. In addition, the number of S phase cells significantly decreased at 12 HAT. The present results indicate that 5AzC induced apoptosis and cell cycle arrest probably at G1 phase in the rat foetal brain and they might be mediated by p53 in response to DNA damage.

Animals↗
PubMed2001

Regulation of differentiation- and proliferation-inducers on Lewis antigens, alpha-fucosyltransferase and metastatic potential in hepatocarcinoma cells.

The expressions of Lewis (Le) antigens, alpha-1,3/1,4 fucosyltransferases (alpha-1,3/1,4 FuTs), and metastatic potential after the treatment of 2 differentiation inducers, all- trans retinoic acid (ATRA), 8-bromo-cyclic 3',5'adenosine monophosphate (8-Br-cAMP); and 2 proliferation inducers, epidermal growth factor (EGF) and phobol-12-myristate-13-acetate (PMA), on 7721 human hepatocarcinoma cell line were studied. Cell adhesion to human umbilical vein endothelial cells (HUVEC), cell migration through transwell and invasion through matrigel were selected as the indexes of metastatic potential-related phenotypes. Using fluorescence-labelled antibodies and flow-cytometric analysis, it was found that 7721 cells mainly expressed sialyl Lewis X (SLe(x)) and a less amount of sialyl dimeric Lewis X (SDLe(x)) antigens on the cell surface. Their expressions were down-regulated by ATRA, and up-regulated by EGF. SLe(x)antigen was also decreased and increased by the treatment of 8-Br-cAMP and PMA respectively. With Northern blot to detect the mRNAs of alpha-1,3/1,4 FuTs, the main enzymatic basis for the change in SLe(x)expression was found to be the alteration of the expression of alpha-1,3 FuT-VII. It was evidenced by the observations that alpha-1,3 FuT-VII was the main alpha-1,3/1,4 FuT in 7721 cells, while alpha-1,3/1,4 FuT-III and alpha-1,3 FuT-VI were expressed rather low. The changes in the expressions of SLe(x)antigen and alpha-1,3 FuT-VII resulted in the altered cell adhesion to tumour necrosis factor-alpha stimulated HUVEC, since only the monoclonal antibody of the SLe(x), but not other monoclonal antibodies blocked the adhesion of 7721 cells to HUVEC. The migration and invasion of 7721 cells were also reduced by the treatment of ATRA or 8-Br-cAMP, and elevated by EGF or PMA. The above findings indicate that the metastatic potential of 7721 cells is suppressed by differentiation-inducers and promoted by proliferation-inducers.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMedDate not supplied

Lead contamination during domestic preparation and cooking of potatoes and leaching of bone-derived lead on roasting, marinading and boiling beef.

Lead concentrations were measured in boiled, mashed potatoes and in baked potatoes that had been prepared and cooked in domestic kitchens. Levels of lead in the boiled, mashed potatoes ranged from below the 1 microgram/kg limit of detection up to 18 micrograms/kg with a mean of 6 micrograms/kg (wet weight). In the large majority of cases the lead in the tap water was the predominant source of the metal. Higher amounts of lead (range 11 micrograms/kg to 56 micrograms/kg, mean 27 micrograms/kg) were present in baked potatoes and this was attributed to soil adhering to the potato skin. The extent of leaching of lead from bone during cooking has also been investigated. For beef stocks there was little evidence to suggest that significant migration of bone lead occurred. For beef casseroles, marinaded in red wine, some leaching did occur from beef joints containing elevated amounts of bone lead; however the levels were all below 350 micrograms/kg and, on average, less than double that found in casseroles prepared from normal joints where the bone lead levels were an order of magnitude less.

Animals↗
PubMed1996

Nitric oxide is necessary for a switch from stationary to locomoting phenotype in epithelial cells.

The restitution of epithelial integrity is accomplished in part by cell migration. Studying this process, we have found that nitric oxide (NO) release migrating epithelial BSC-1 cells displayed a biphasic response to the inflicted wounds; an initial transient release of NO is followed by a delayed sustained elevation. Whereas the constitutive endothelial NO synthase (NOS) did not show any spatial or temporal changes associated with wounding, the inducible NOS became expressed 3 h after wounding and showed higher abundance at the edges of epithelial wounds. L-Arginine (L-Arg) or NO donor, S-nitroso-N-acetyl-DL-penicillamine, exerted motogenic effect in epithelial and endothelial cells. Inhibition of NOS with NG-nitro-L-arginine methyl ester (L-NAME) or a selective knockout of inducible NOS with antisense oligodeoxynucleotides reduced the rate of spontaneous or epidermal growth factor (EGF)-induced BSC-1 cell migration. Migrating cells showed the polarized expression of NOS, suggesting a head-to-rear NO gradient. Several growth factors (EGF, insulin-like growth factor I, hepatocyte growth factor, and fibroblast growth factor) were motogenic for BSC-1 cells, but this effect was abrogated by pretreatment with L-NAME. We conclude that endogenous NO production is a prerequisite for BSC-1 cell migration. A vectorial NO release may be essential for the spatially and temporally coordinated reciprocal phenomena that occur at the leading and trailing edge of locomoting epithelial cells. Although the exact mode of NO action remains uncertain, it is conceivable that the production of NO serves as a cellular switch from the stationary to the locomoting epithelial phenotype.

Animals↗
PubMed2002

Calcineurin in human heart hypertrophy.

BACKGROUND: In animal models, increased signaling through the calcineurin pathway has been shown to be sufficient for the development of cardiac hypertrophy. Calcineurin activity has been reported to be elevated in the myocardium of patients with congestive heart failure. In contrast, few data are available about calcineurin activity in patients with pressure overload or cardiomyopathic hypertrophy who are not in cardiac failure. METHODS AND RESULTS: We investigated calcineurin activity and protein expression in 2 different forms of cardiac hypertrophy: hypertrophic obstructive cardiomyopathy (HOCM) and aortic stenosis (AS). We found that the C-terminus of calcineurin A protein containing the autoinhibitory domain was less abundant in myocardial hypertrophy than in normal heart, which suggests the possibility of proteolysis. No new splice variants could be detected by reverse-transcription polymerase chain reaction. This resulted in a significant elevation of calcineurin enzymatic activity in HOCM and AS compared with 6 normal hearts. Increased calcineurin phosphatase activity caused increased migration of NF-AT2 (nuclear factor of activated T cells 2) in SDS-PAGE compatible with pronounced NF-AT dephosphorylation in hypertrophied myocardial tissue. CONCLUSIONS: Hypertrophy in HOCM and AS without heart failure is characterized by a significant increase in calcineurin activity. This might occur by (partial) proteolysis of the calcineurin A C-terminus containing the autoinhibitory domain. Increased calcineurin activity has functional relevance, as shown by altered NF-AT phosphorylation state. Although hypertrophy in AS and HOCM may be initiated by different upstream triggers (internal versus external fiber overload), in both cases, there is activation of calcineurin, which suggests an involvement of this pathway in the pathogenesis of human cardiac hypertrophy.

Aortic Valve Stenosis↗
PubMed1979

Cancer patterns in the oil shale area of the Estonian S.S.R.

Age-adjusted incidence rates of stomach, lung, and skin cancer among urban (1967-1972) and rural (1963-1972) population of four administrative districts in the Estonian S.S.R. have been presented. In the Kohtla-Järve district (oil shale area) there was an excess of stomach and lung cancer. High rates of stomach cancer in towns and boroughs of oil shale area may be explained by migration. A great proportion of migrants comes from regions, where incidence rates are 1.6-2.5. times higher than among estonians. Elevated levels of stomach cancer incidence in rural areas of Kohtla-Järva district remained unexplainable. In a retrospective cohort study of 2069 workers who had been exposed to oil shale products from 10 to 20 years an excess of skin cancer in females was found.

Emigration and Immigration↗
PubMedDate not supplied

[The role of corticosteroids in regulation of cell migration in emotional-pain stress].

It was found that an increase in the adrenocortical and blood plasma 11-HOCS concentration is seen immediately after emotional-pain stress (EPS) and 72 to 96 hours following stress affection. An intensified thymic and splenic repopulation by cells, migrating from the bone marrow, occurs during the interval between 48 and 192 hours following EPS. It was suggested that elevation of the corticosteroid level in the organism in late periods after stress is directed to the cell population recovery.

11-Hydroxycorticosteroids↗
PubMed1998

[Vascular endothelial cells and renin-angiotensin system].

The vascular renin-angiotensin system (RAS) is regulated independently from circulating RAS and plays a role in the local regulation of vascular tone, the modulation of sympathetic activity and vascular remodeling. Endothelial cells are a major source of angiotensin converting enzyme (ACE), which produces angiotensin II and degrades bradykinin, in normal arteries. Mechanical stress such as transmural pressure, stretch stress and shear stress appear to contribute to the regulation of endothelial ACE activity. In contrast, vessels with intimal proliferation such as atheromatous plaque and neointima following balloon injury show expression of ACE in smooth muscle cells and macrophages in the intimal lesions. Activation of ACE in intimal SMC may relate to a phenotypic change of SMC from the contracting type of the synthetic type. Activation of ACE in macrophages is also related to the transformation of macrophages from monocytes. Concerning the role of the activated RAS, elevated blood pressure and vascular tonus by angiotensin II are candidates of vascular injury and plaque rupture. Angiotensin II stimulates migration and proliferation of smooth muscle cells and production of extracellular matrix. Furthermore, angiotensin II increases oxidized-LDL which may be related to the forming of macrophages. These evidence suggest that activation of vascular RAS following endothelial dysfunction/injury play an important role in the pathogenesis of vascular remodeling and atherosclerosis.

Animals↗
PubMed1998

Novel splice variants of human tenascin-C mRNA identified in normal and bullous keratopathy corneas.

PURPOSE: Pseudophakic/aphakic bullous keratopathy (PBK/ABK) human corneas accumulate an extracellular matrix glycoprotein tenascin-C (TN-C), an important modulator of cell adhesion and migration. Here, the purpose was to identify specific TN-C mRNA splice variants in normal and PBK/ABK human corneas. METHODS: Conventional and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) with primers to alternatively spliced (insertional) and constitutive fibronectin type II-like repeats of TN-C was used. Splice variants were identified by cloning and sequencing of RT-PCR products or by Southern blot analysis. RESULTS: The majority of corneal TN-C mRNA species corresponded to relatively small forms of the protein. Four previously unidentified TN-C mRNA splice variants were found in normal and PBK/ABK corneas that contained insertional repeats A1+A2+B+D, A1+A2+D, A1+B+D, or A1+D. Variants with insertional repeats A1+A2 or A1, previously described in mouse and rat, were also identified in human corneas. Semiquantitative RT-PCR showed that novel TN-C mRNA variants were dramatically elevated in PBK/ABK compared to normal corneas. CONCLUSION: TN-C protein was found in PBK/ABK but not in normal corneas; however, both normal and diseased corneas contained mRNA for 15 different TN-C isoforms. PBK/ABK corneas had elevated levels of six relatively small TN-C mRNA variants including five novel ones. These specific isoforms may adversely affect adhesion and migration of corneal cells thus contributing to the exacerbation of PBK/ABK.

Alternative Splicing↗