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J D Taylor

Publications and source records attributed to J D Taylor.

At least 37 records · Page 2Linked to original sources

Nonlethal gamma radiation displays similar cytoplasmic rearrangements as 12(S)-HETE.

Timar et al. (Int. J. Canc., 52:594-603, 1992) and Onoda et al. (Rad. Res., 130:281-288, 1992) implicated 12(S)-HETE and nonlethal gamma radiation respectively, in enhanced expression of the alpha IIb beta 3 integrin receptor in B16a tumor cells. 12(S)-HETE has been reported to induce rearrangement of cytoplasmic elements and movement of cytoplasm (Haddad and Taylor, Proc. Amer. Cancer Res., 34:51, 1993); Timar et al., Cell Motil. Cytoskel., 26:49-65, 1993). Here, we report similar results in B16a tumor cells by post 90 cGy gamma radiation. Control cells were circular without cytoplasmic processes with the majority of their organelles and elements in perinuclear regions both surrounded by a ring of actin microfilaments. The cell's extensive leading edge was organelle free with the exception of occasional endoplasmic reticular cisternae parallel to one or two microtubules, and short bundles of actin microfilaments perpendicular to the plasma membrane. As early as 5 sec, but better defined by 60-90 sec, one end of elongated microfilaments bundles became associated with the plasma membrane while the other end of the bundles became associated with perinuclear mass protrusions. By 5 min, prominent by 15 min, protrusions, now separated from the leading edge by mixture of bundle and ring microfilaments, reached the plasma membrane to form cellular processes. By 30 min, some cytoplasmic masses showed signs of retraction along with the disappearance of their associated mixed microfilaments. As well as numerous vesicles of unknown origin, primarily associated with microtubules perpendicular to the plasma membrane, mitochondria and endoplasmic reticular cisternae were found in the cytoplasmic masses.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

12(S)-hydroxyeicosatetraenoic acid and 13(S)-hydroxyoctadecadienoic acid regulation of protein kinase C-alpha in melanoma cells: role of receptor-mediated hydrolysis of inositol phospholipids.

Protein kinase C (PKC) isoenzymes are essential components of cell signaling. In this study, we investigated the regulation of PKC-alpha in murine B16 amelanotic melanoma (B16a) cells by the monohydroxy fatty acids 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] and 13(S)-hydroxyoctadecadienoic acid [13(S)-HODE]. 12(S)-HETE induced a translocation of PKC-alpha to the plasma membrane and focal adhesion plaques, leading to enhanced adhesion of B16a cells to the matrix protein fibronectin. However, 13(S)-HODE inhibited these 12(S)-HETE effects on PKC-alpha. A receptor-mediated mechanism of action for 12(S)-HETE and 13(S)-HODE is supported by the following findings. First, 12(S)-HETE triggered a rapid increase in cellular levels of diacylglycerol and inositol trisphosphate in B16a cells. 13(S)-HODE blocked the 12(S)-HETE-induced bursts of both second messengers. Second, the 12(S)-HETE-increased adhesion of B16a cells to fibronectin was sensitive to inhibition by a phospholipase C inhibitor and pertussis toxin. Finally, a high-affinity binding site (Kd = 1 nM) for 12(S)-HETE was detected in B16a cells, and binding of 12(S)-HETE to B16a cells was effectively inhibited by 13(S)-HODE (IC50 = 4 nM). In summary, our data provide evidence that regulation of PKC-alpha by 12(S)-HETE and 13(S)-HODE may be through a guanine nucleotide-binding protein-linked receptor-mediated hydrolysis of inositol phospholipids.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

A cyclic adenosine 3',5'-monophosphate signal is required for the induction of IL-1 beta by TNF-alpha in human monocytes.

IL-1 beta is a cytokine generally considered to be a major component involved in the pathogenesis of rheumatoid arthritis and other inflammatory diseases. Of the agents found in high concentrations in inflamed rheumatoid arthritis joints, TNF-alpha is among the most strongly implicated as an in vivo inducer of IL-1 beta. Here we report that in human PBMC and in a stable transfectant of the promonocytic cell line, THP-1, TNF-alpha indeed appears to be an inducer of IL-1 beta production, but only in the presence of dibutyryl cAMP or agents such as the PG that elevate intracellular cAMP levels. This TNF-alpha/cAMP pathway regulates IL-1 beta production at the level of transcription and requires a cAMP response element located between -2762 and -2755 bp in the upstream regulatory sequence of IL-1 beta. Because PG, which are known to elevate cAMP levels in vivo, and TNF-alpha are both found in significant quantities in the synovial fluid of rheumatoid arthritis joints, the observed synergistic up-regulation in IL-1 beta synthesis by TNF-alpha/cAMP (PG) may provide valuable insight into the potential pathways involved in the continuous production of IL-1 beta in the chronically inflamed joint.

Alkaline Phosphatase↗

Ultrastructural immunogold localization of some organelle-transport relevant proteins in wholemounted permeabilized nonextracted goldfish xanthophores.

By whole-cell transmission electron microscopy (WCTEM), we recently demonstrated that carotenoid droplets are transported by elongating or retracting endoplasmic reticular cisternae in goldfish xanthophores. Here we report that permeabilized xanthophores demonstrate immunogold reactivity against several proteins involved in organelle translocation. The gold labeling against beta-tubulin and the intermediate filament protein p45a were found on microtubules and intermediate filaments. Labeling with anti-actin was found on nonidentifiable structures, on vesicles of unknown origin, occasional labeling on carotenoid droplets, and on occasional microfilaments. Immunoreactivity was demonstrated with anti-p57 on the carotenoid droplet surface, confirming previous results (Lynch et al., 1986a,b). Labeling with anti-PCD6 subunit (of the inositol trisphosphate/ryanodine receptor) was demonstrated on carotenoid droplets suggesting they possess calcium channels. Anti-MAP 1C (dynein) immunolabeling was generally seen on club-shaped structures in the cytomatrix and on carotenoid droplets. Finally, immunogold labeling with anti-MAP 2a + 2b was seen on a meshwork of microfilaments and intermediate filaments. Finally, this is the first report of a WCTEM technique for permeabilized cells that reveals immunoreactive elements, organelles, and cytomatrix components without the additional requirements of extraction or fracturing.

Animals↗

Immunomorphological characterization and effects of 12-(S)-HETE on a dynamic intracellular pool of the alpha IIb beta 3-integrin in melanoma cells.

In metastatic B16a murine melanoma cells, alpha IIb beta 3 integrin was shown to be one of the key adhesion molecules responsible for matrix adhesion and spreading. Upon stimulation, alpha IIb beta 3 can be upregulated at the cell surface due to translocation of the receptor to the plasma membrane from an intracellular pool. Here we have characterized this integrin pool as a tubulovesicular structure (TVS) corresponding to endosomes. TVS was found to be associated temporarily with microtubules and intermediate filaments especially after protein kinase C (PKC) stimulation with a lipoxygenase metabolite of arachidonic acid, 12-(S)-hydroxyeicosatetraenoic acid [12-(S)-HETE]. After PKC stimulation, the predominantly vesicular TVS became elongated and alpha IIb beta 3 appeared at the apical plasma membrane and microvilli. Disruption of either the microtubules or intermediate filaments prevented the 12-(S)-HETE effect both on vesicular to tubular transition of TVS as well as on surface expression of this integrin. The connection with the Golgi system of the integrin-containing TVS was proved by a Golgi-inhibitor (brefeldin A) pretreatment, which prevented the PKC-stimulation-induced TVS elongation and subsequent receptor-upregulation at the cell surface. After a soluble ligand binding (mAb to the alpha IIb beta 3 complex) the surface receptor endocytosed back to the TVS indicating the presence of a dynamic, cytoskeleton associated integrin pool in melanoma cells.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Differential regulation of human monocyte-derived TNF alpha and IL-1 beta by type IV cAMP-phosphodiesterase (cAMP-PDE) inhibitors.

Elevation of cAMP downregulates certain functions of inflammatory cells, including the release of TNF alpha and IL-1 beta by macrophages. Intracellular cAMP levels can be modulated pharmacologically by adding cell-permeable cAMP analogs, by stimulating adenylate cyclase or by inhibiting degradation of cAMP by cAMP-phosphodiesterases (cAMP-PDE). Multiple forms of cAMP-PDEs have been identified in various tissues and cells using both biochemical characterization and selective inhibitors. Therefore, we wanted to determine which of these different PDE isoforms was present in human monocytes and whether this isoform could regulate cytokine release from human monocytes by a mechanism similar to that seen with dbcAMP or PGE1. Our results demonstrate that selective inhibitors of type IV cAMP-PDE, such as rolipram and Ro20-1724, are clearly the most effective compounds at enhancing cAMP levels and inhibiting the release of TNF alpha and IL-1 beta in these cells. The type III cAMP-PDE-selective inhibitors C1930 and cilostamide and the nonselective PDE inhibitors IBMX and pentoxifylline were significantly less potent. In agreement with these data, cAMP-PDE activity in cytosolic extracts from human monocytes was also much more sensitive to inhibition by rolipram than by cilostamide. Additionally, rolipram dramatically reduced TNF alpha mRNA accumulation, which supports previous findings that cAMP regulates TNF alpha at the transcriptional level. Surprisingly, rolipram, rolipram, dbcAMP or PGE1 increased IL-1 beta was reduced, which indicates that cAMP can have both positive and negative effects on the regulation of IL-1 beta.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗

Determination of urinary albumin using high-performance immunoaffinity chromatography and flow injection analysis.

The detection of low levels of albumin in urine can be an important aid in the early diagnosis of kidney disease. In this study, an automated system for urine analysis was developed that could simultaneously measure both albumin and creatinine, an indicator of urine output and volume. Albumin was determined by use of a column that contained immobilized anti-albumin antibodies. An on-line flow injection analysis system was used to measure creatinine as this solute eluted nonretained from the antibody column. The total analysis time of the system was 5 min per injection. Limits of detection for albumin and creatinine in a 20 microL sample (at S/N = 2) were 3 and 5 mg/L, respectively. The response for these compounds covered the range of clinical interest. Within-run precision for both analytes was +/- 1-2% at normal urine concentrations. The results of this method showed good agreement with those obtained by reference techniques. This approach can be adapted for the detection of other urine components by changing the type of antibody column used in the system.

Albuminuria↗

Descriptive epidemiology of prostate cancer in metropolitan Detroit.

BACKGROUND: The incidence of prostate cancer among US men increased more than five times over the past six decades. Black men in the United States now have the world's highest reported incidence of prostate cancer. The authors examined the distribution of prostate cancer in metropolitan Detroit from 1973 to 1989. METHODS: Cases collected by the Metropolitan Detroit Cancer Surveillance System were used to calculate standardized age-adjusted rates of prostate cancer by race and stage and standardized age-specific rates for the age groups 60-69, 70-79 and 80 years and older. Over 24,000 cases involving black and white men were analyzed. RESULTS: During 1973 to 1989, age-adjusted rates of prostate cancer diagnosed among white men doubled from 54.3 to 109.9 per 100,000 and those among black men increased by nearly 40% from 106.9 to 148.6 per 100,000. Average annual increases in age-adjusted rates for white and black men were 4.4 and 2.3%, respectively. CONCLUSIONS: Age-adjusted rates of prostate cancer diagnosed among white men increased more rapidly than rates among black men during 1973 to 1989. The more rapid increase in cases diagnosed in white men may represent differences in access and exposure to early detection and treatment practices. Improved efforts toward earlier detection are needed, especially among black men.

Age Factors↗

Goldfish tyrosinase related protein I (TRP-1): deduced amino acid sequence from cDNA and comments on structural features.

Previous workers have shown that mammals have tyrosinase and tyrosinase related proteins (TRPs) that share common structural domains, all of which are not present in microbial tyrosinases. We report here the deduced amino acid sequence of a TRP from fish that is highly homologous to mammalian TRP-1. Examination of the structures of these vertebrate tyrosinases and TRPs shows that, aside from the conserved cysteine-rich and histidine-rich domains previously noted, there are a large number of conserved prolines and glycines, leading to an abundance of turns and few conserved helical regions. These tyrosinases and TRP-1s also have in their cytosolic tails a consensus sequence that is not present in any other protein. It is proposed that this sequence may participate in directing these proteins to the melanosomes.

Amino Acid Sequence↗

Polyarthritis in wild mice (Mus musculus) caused by Streptobacillus moniliformis.

Mice trapped on farms in south-eastern Queensland had chronic abscessating osteoarthritides mainly involving the carpi and tarsi. Pleomorphic bacteria were shown by silver staining to be plentiful within lesions. Streptobacillus moniliformis was isolated from the joints, and streptobacillary polyarthritis was diagnosed. Other lesions observed included subcutaneous and hepatic abscesses.

Abscess↗