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PubMed2003

Amyloid processing and signal transduction properties of antiparkinson-antialzheimer neuroprotective drugs rasagiline and TV3326.

Two novel neuroprotective cholinesterase (ChE) inhibitors, TV3326 and TV3279 [(N-propargyl-(3R) and (3S) aminoindan-5-yl)-ethyl methyl carbamate], respectively were derived from rasagiline, for the treatment of Alzheimer's disease (AD). TV3326 also inhibits monoamine oxidase (MAO)-A and B, while its S-isomer, TV3279, lacks MAO-inhibitory activity. The actions of these drugs in the regulation of the amyloid precursor protein (APP) processing using rat PC12 and human SH-SY5Y neuroblastoma cells were examined. Both isomers stimulated the release of the non-amyloidogenic alpha-secretase form of soluble APP (sAPPalpha) from these cell lines. The increases in sAPPalpha, induced by TV3326 and TV3279, were dose-dependent (0.1-100 micro M) and blocked by the hydroxamic acid-based metalloprotease inhibitor, Ro31-9790, suggesting mediation via alpha-secretase activity. Using several signal transduction inhibitors, the involvement of protein kinase C (PKC), mitogen-activated protein (MAP) kinase, and tyrosine kinase-dependent pathways in the enhancement of sAPPalpha release by TV3326 and TV3279 was identified. In addition, both drugs directly induced the phosphorylation of p44 and p42 MAP kinase, which was abolished by the specific inhibitors of MAP kinase activation, PD98059 and U0126. These data suggest a novel pharmacological mechanism, whereby these ChE inhibitors regulate the secretary processes of APP via activation of the MAP kinase pathway.

Alzheimer Disease↗

PubMed2006

Differential roles of MAP kinases in atorvastatin-induced VEGF release in cardiac myocytes.

Statins, specific inhibitors of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, are now widely used for treatment of patients with hypercholesterolemia. In addition to the reduction of cholesterol biosynthesis, accumulating evidence indicates that statins have several pleiotropic effects especially on cardiovascular system. However, the exact role of statin in cardiac myocytes remains unclear. In the present study, we investigated whether atorvastatin induces vascular endothelial growth factor (VEGF) release in cardiac myocytes, and the underlying mechanism. We observed that atorvastatin significantly stimulated VEGF release in a dose-dependent manner. It induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase but not SAPK (stress-activated protein kinase)/JNK (c-Jun N-terminal kinase). The atorvastatin-induced VEGF release was enhanced by PD98059, which is a specific inhibitor of the upstream kinase that activates p44/p42 MAP kinase (MEK). Further, it was significantly reduced by SB203580, a specific inhibitor of p38 MAP kinase. Furthermore, the atorvastatin-induced phosphorylation of p38 MAP kinase was attenuated by SB203580, whereas it was enhanced by PD98059. Taken together, these results suggest that the atorvastatin-induced VEGF release in cardiac myocytes is positively regulated by p38 MAP kinase and negatively regulated byp44/p42 MAP kinase and that the atorvastatin-induced phosphorylation of p38 MAP kinase is regulated by p44/p42 MAP kinase in these cells.

Animals↗

PubMed1999

A novel LPS-inducible C-type lectin is a transcriptional target of NF-IL6 in macrophages.

C-type lectins serve multiple functions through recognizing carbohydrate chains. Here we report a novel C-type lectin, macrophage-inducible C-type lectin (Mincle), as a downstream target of NF-IL6 in macrophages. NF-IL6 belongs to the CCAAT/enhancer binding protein (C/EBP) of transcription factors and plays a crucial role in activated macrophages. However, what particular genes are regulated by NF-IL6 has been poorly defined in macrophages. Identification of downstream targets is required to elucidate the function of NF-IL6 in more detail. To identify downstream genes of NF-IL6, we screened a subtraction library constructed from wild-type and NF-IL6-deficient peritoneal macrophages and isolated Mincle that exhibits the highest homology to the members of group II C-type lectins. Mincle mRNA expression was strongly induced in response to several inflammatory stimuli, such as LPS, TNF-alpha, IL-6, and IFN-gamma in wild-type macrophages. In contrast, NF-IL6-deficient macrophages displayed a much lower level of Mincle mRNA induction following treatment with these inflammatory reagents. The mouse Mincle proximal promoter region contains an indispensable NF-IL6 binding element, demonstrating that Mincle is a direct target of NF-IL6. The Mincle gene locus was mapped at 0.6 centiMorgans proximal to CD4 on mouse chromosome 6.

Animals↗

PubMed1994

An enhancer core element mediates stimulation of the rat beta-myosin heavy chain promoter by an alpha 1-adrenergic agonist and activated beta-protein kinase C in hypertrophy of cardiac myocytes.

In hypertrophy of cultured rat cardiac myocytes, alpha 1-adrenergic agonists activate protein kinase C (PKC) and up-regulate beta-myosin heavy chain (MHC). The 3300-base pair (bp) rat beta-MHC promoter is stimulated by both an alpha 1-agonist and a constitutively activated mutant of beta-PKC (Kariya, K., Karns, L. R., Simpson, P. C. (1991) J. Biol. Chem. 266, 10023-10026). Here, we report the convergence of alpha 1-adrenergic and beta-PKC signaling on the same element of the beta-MHC promoter. A 20-bp sequence in the beta-MHC promoter (-215/-196) was required for induction by both alpha 1-adrenergic stimulation and beta-PKC and conferred induction on a heterologous promoter. This sequence bound myocyte nuclear factor(s) through a 9-bp "enhancer core" (5'-TGTGGTATG-3'). A 3-bp mutation within the enhancer core which abolished factor binding also abolished inducibility of a 215-bp beta-MHC promoter. These results support the idea that beta-PKC is in the pathway for alpha 1-adrenergic regulation of beta-MHC transcription during cardiac myocyte hypertrophy. The enhancer core is the first PKC response element mapped by transfection of an activated PKC mutant, rather than by treatment with phorbol esters.

Animals↗

PubMed2006

Noladin ether acts on trabecular meshwork cannabinoid (CB1) receptors to enhance aqueous humor outflow facility.

PURPOSE: To study the effects of 2-arachidonyl glyceryl ether (noladin ether), an endocannabinoid ligand selective for cannabinoid (CB)1 receptor, on aqueous humor outflow facility, to investigate the involvement of trabecular meshwork CB1 receptors and the p42/44 MAP kinase signaling pathway and to explore the cellular mechanisms of noladin ether-induced changes of outflow facility. METHODS: The effects of noladin ether on aqueous humor outflow facility were measured in a porcine anterior-segment-perfused organ culture model. The expression of CB1 receptors on cultured porcine trabecular meshwork cells and the coupling of these receptors to p42/44 MAP kinase was determined by immunofluorescence microscopy and Western blot analysis. Both Western blot and zymography were used to monitor the effects of noladin ether on matrix metalloproteinase (MMP)-2. In morphologic studies, AlexaFluor 488-labeled phalloidin staining was used to examine actin filament, and immunohistochemistry with anti-paxillin antibodies was used to detect focal adhesions. RESULTS: Within 1 hour after adding 3, 30, or 300 nM of noladin ether, the aqueous humor outflow facility increased concentration dependently. The effect of 30 nM of noladin ether was completely blocked by SR141716A, a selective CB1 antagonist. Positive signals were detected on cultured porcine trabecular meshwork cells with an anti-CB1 antibody in immunofluorescence microscopy and Western blot studies. Treatment of trabecular meshwork cells with 30 nM of noladin ether activated p42/44 MAP kinase, whereas pretreatment with SR141716A blocked the p42/44 MAP kinase-activating effects of noladin ether. In addition, the enhancement of outflow facility induced by noladin ether was blocked by pretreatment of porcine anterior segments with PD98059, an inhibitor of p42/44 MAP kinase pathway. Furthermore, noladin ether treatment caused rounding of trabecular meshwork cells, and there was a decrease of actin stress fibers, as well as a decrease in focal adhesions. These noladin ether-induced morphologic changes were also blocked by SR141716A and PD98059. CONCLUSIONS: The results demonstrate for the first time that administration of noladin ether, an endocannabinoid agonist selective for the CB1 receptor, increases aqueous humor outflow facility. The data also show that noladin ether-induced enhancement of outflow facility is mediated through the trabecular meshwork CB1 receptor, with an involvement of p42/44 MAP kinase signaling pathway and changes in actin cytoskeletons.

Actins↗

PubMed2004

Intracranial pyogenic abscess: imaging diagnosis utilizing recent advances in computed tomography and magnetic resonance imaging.

Intracranial abscesses are life-threatening medical emergencies with pyogenic debris accumulating in the brain. Delay in the diagnosis can result in significant morbidity and mortality. Computed tomography and magnetic resonance imaging play an important role in the diagnosis of brain abscesses. However, the classic ring-enhancing appearance of an intracranial abscess can be mimicked by several other entities, most notably a necrotic tumor. This paper reviews new advances in CT and MR for imaging patients with suspected brain abscess. The role of computed tomography (CT) perfusion and new magnetic resonance sequences including DWI sequences, ADC map, MR spectroscopy, FLAIR and post-contrast enhanced T1 weighted images will also be discussed.

Brain Abscess↗

PubMed2005

CCAAT/enhancer binding protein epsilon: changes in function upon phosphorylation by p38 MAP kinase.

C/EBPepsilon, a member of the CCAAT/enhancer binding protein family, is a transcription factor important in neutrophil differentiation. We have determined that it is phosphorylated on multiple serine and threonine residues and can be a target for phosphorylation by a number of kinases. We identified a threonine at amino acid 75, part of a consensus mitogen-activated protein (MAP) kinase site within the transactivation domain of C/EBPepsilon, as being phosphorylated only by p38 MAP kinase. Phosphorylation of this residue resulted in enhanced transcriptional activity on a myeloid-specific promoter in in vitro transient transfection reporter assays. We also determined that phosphorylation at Thr75 yielded a protein that was more effective at binding its cognate DNA sequence compared with the wild-type nonphosphorylated C/EBPepsilon. Stable expression of C/EBPepsilonT75A in interleukin 3 (IL-3)-dependent 32Dcl3 did not result in the up-regulation of expression of secondary granule genes compared with wild-type C/EBPepsilon or C/EBPepsilonT75D. Therefore we suggest that C/EBPepsilon is a target for p38 MAP kinase activity.

CCAAT-Enhancer-Binding Proteins↗

PubMed1998

Response of MCF7 human breast cancer to tamoxifen: evaluation by the three-time-point, contrast-enhanced magnetic resonance imaging method.

Variations in the cellular volume fraction and in the microvascular permeability of MCF7 human breast tumors were used to assess response to tamoxifen. These pathophysiological features were mapped by applying the three-time-point, contrast-enhanced, high resolution magnetic resonance imaging method (H. Degani et al, Nat. Med., 3: 780-782, 1997). Short-term treatment with tamoxifen caused a highly significant increase in the fraction of pixels displaying intermediate contrast agent clearance pattern and a significant increase in the fraction of pixels displaying high rate of contrast agent entrance. These changes resulted from a marked rise in the extracellular volume fraction, indicating increased necrosis, and from an augmentation in the microvascular permeability, predominantly in the vicinity of the high extracellular volume fraction areas, as a result of stress-induced angiogenesis.

Breast Neoplasms↗

PubMed2001

Chronic hypoxia induces constitutive p38 mitogen-activated protein kinase activity that correlates with enhanced cellular proliferation in fibroblasts from rat pulmonary but not systemic arteries.

Pulmonary hypertension occurs commonly in patients with chronic hypoxic lung disease and is characterized by the remodeling of the pulmonary artery walls. The molecular mechanisms underlying such remodeling are unknown but we have recently shown that the stress-activated (Jnk and p38) mitogen-activated protein (MAP) kinases are activated in pulmonary artery fibroblasts following acute hypoxia. We now show that Erk and p38 MAP kinases are constitutively activated in fibroblasts derived from the remodeled pulmonary, but not the systemic circulation from rats exposed to chronically hypoxic conditions. Moreover, we find that such fibroblasts show sustained enhanced proliferative capacities relative to pulmonary artery fibroblasts derived from normoxic rats or to aortic fibroblasts from either normoxic or hypoxic rats. Finally, abrogation of p38, but not Erk MAP kinase activity by use of specific inhibitors, prevents the enhanced proliferative capacity exhibited by pulmonary artery fibroblasts. Taken together, these data suggest that enhanced p38 MAP kinase activity provides a molecular mechanism to explain the proliferation of pulmonary artery fibroblasts required for remodeling of the pulmonary vasculature.

Animals↗

PubMed2002

The neural cell adhesion molecule L1 potentiates integrin-dependent cell migration to extracellular matrix proteins.

The L1 adhesion molecule regulates axon growth and is mutated in the X-linked mental retardation syndrome CRASH (acronym for corpus callosum agenesis, retardation, aphasia, spastic paraplegia, hydrocephalus). A novel role for L1 as a potentiator of neuronal cell migration to extracellular matrix proteins through beta1 integrins and intracellular signaling to mitogen-activated protein (MAP) kinase was identified. L1 potentiated haptotactic migration of B35 neuroblastoma cells toward fibronectin, vitronectin, and laminin through the signaling intermediates c-Src, phosphatidylinositol-3 kinase, and MAP kinase. L1 potentiated migration toward fibronectin through alpha5beta1 integrin in human embryonic kidney 293 cells and depended on determinants of L1 endocytosis: dynamin I, c-Src, and the AP2/clathrin binding site (Arg-Ser-Leu-Glu) in the neuronal splice form of L1. L1 clustering on the cell surface enhanced the internalization of activated beta1 integrins and L1 into distinct endocytic vesicles. L1-potentiated migration, enhancement of beta1 integrin endocytosis, and activation of MAP kinase were coordinately inhibited by mutation of an RGD sequence in the sixth immunoglobulin-like domain of L1. Moreover, three CRASH mutations in the L1 cytoplasmic domain (1194L, S1224L, Y1229H), two of which interfere with ankyrin association, inhibited L1-potentiated migration and MAP kinase activation. Function-blocking antibodies to L1 and beta1 integrin retarded the migration of 5-bromo-2'-deoxyuridine-labeled mouse cerebellar granule cells in slice cultures, underscoring the potential physiological relevance of these findings. These studies suggest that L1 functionally interacts with beta1 integrins to potentiate neuronal migration toward extracellular matrix proteins through endocytosis and MAP kinase signaling, and that impairment of this function by L1 cytoplasmic domain mutations may contribute to neurological deficits in CRASH.

Animals↗

PubMed2004

Putative intestine-specific enhancers located in 5' sequence of the CDX1 gene regulate CDX1 expression in the intestine.

CDX1 is a homeobox transcription factor that plays a critical role in intestinal epithelial cell growth and differentiation. CDX1 gene expression is tightly regulated in a temporal and cell-type specific manner. However, very little is known about the regulatory mechanisms that direct CDX1 gene expression in the intestine. To elucidate these mechanisms, we employed a series of transgenic mouse studies using the 5' flanking sequences of the human CDX1 gene. Transgenic mice containing nucleotides between -5667 and +68 relative to the transcription start site of the CDX1 gene demonstrated ectopic expression of the transgene in the brain and gastric smooth muscle. However, transgenic expression of the nucleotides -15601 to +68 of the CDX1 gene was restricted to the intestinal epithelium, which was identical to endogenous CDX1 gene expression. Taken together, the upstream sequences between -15601 and -5667 contain regulatory elements that direct transgene expression specifically to the intestinal epithelium. Furthermore, DNase I hypersensitivity assays revealed two active chromatin regions in the CDX1 gene (hypertensive sites 1 and 2) located at approximately -5.8 and -6.8 kb upstream of the CDX1 gene, respectively, which may function as potential intestine-specific enhancers.

Animals↗

PubMed1996

Microtubule-associated proteins regulate microtubule function as the track for intracellular membrane organelle transports.

Axonal microtubules have two essential roles: providing the track for organelle transport and forming the cytoskeletal framework to maintain axonal morphology. Microtubule-associated proteins (MAPs) are essential for the formation of cytoskeletal architecture. However, they may have additional roles on the regulation of organelle transport by their interaction with motor proteins on the microtubules. We first examined the effects of axonal MAPs on the organelle movement along microtubules in a heterologous system using COS fibroblasts, which express no axonal MAPs, such as tau or MAP2C. Transfection of tau or MAP2C gene suppressed organelle movement almost completely in this cell type, hence interaction of axonal MAPs with microtubules interferes with organelle transports. It is known that the phosphorylation of MAPs reduces their interaction with microtubules. In this sense, phosphorylation of MAPs can be a good candidate for the molecular switch to regulate the organelle transport. As a second set of experiments, we investigated the effects of modulating cAMP dependent protein kinase pathway on organelle transports in primary sensory neurons, where high-molecular-weight tau protein is the major MAP. We found that the application of dibutyryl cAMP enhanced transports of large organelles in the axon. Furthermore, this drug treatment phosphorylated endogenous tau protein and thus reduced the affinity of tau to microtubules. These results indicate that axonal MAPs can work as a phosphorylation-dependent regulator of organelle transport. Local activation of protein kinase pathways in the axon might play an important role on the segregation of microtubules serving for either organelle transport or cytoskeletal architecture.

Animals↗

PubMed1999

Identification of a novel enhancer sequence in the distal promoter of the rat fatty acid synthase gene.

The proximal promoter and first intron of the fatty acid synthase (FAS) gene contains response sequences for insulin and glucose, but the 2- to 3-fold increase in FAS promoter activity attributable to these sequences falls short of the 20- to 30-fold induction in hepatic FAS gene transcription observed in fasted-refed rats. Using DNase I hypersensitivity site (HSS) mapping, two new liver specific sites were localized to the regions of: -8600 to -8500 (HSS 1) and -7300 to -7000 (HSS 2). DNase sensitivity of the -7300 to -7000 region was increased when fasted rats were refed glucose. When rat hepatocytes were transfected with a CAT construct that linked the region of -9700 and -4606 with the insulin response region located between -265 to +65, FAS promoter activity was induced 15-fold. This increase required the presence of both insulin and glucocorticoids. Deleting HSS 2 abolished the 15-fold induction in FAS promoter activity, but removing HSS 1 was without effect. Apparently the in vivo regulation of hepatic FAS gene transcription requires response elements located in the region of -7300 to -7000 and -265 to +65.

Animals↗

PubMed1987

The enhancer of the immunoglobulin heavy chain locus is flanked by presumptive chromosomal loop anchorage elements.

We have located presumptive chromosomal loop anchorage elements within the mouse heavy chain immunoglobulin locus. Analysis of 31 kilobases spanning diversity, joining, enhancer, switch, and the mu and delta constant regions reveals that only a single 1-kilobase segment exhibits specific binding to nuclear matrices. It is of particular significance that the transcriptional enhancer element resides within this matrix association region (MAR). Fine structure mapping indicates that binding is mediated by A+T-rich approximately 350-base pair segments that reside on either side of the enhancer. The MAR sequences residing 5' of the enhancer contain topoisomerase II consensus sequences like the MAR located upstream of the kappa light chain gene enhancer. The heavy chain gene MARs, however, exhibit a lower affinity for matrix association compared to the kappa gene MAR. Significantly, the juxtaposition of enhancer elements with MARs appears to be evolutionarily conserved within the immunoglobulin genes, suggesting that MARs may act as positive and/or negative regulators of enhancer function.

Animals↗

PubMedDate not supplied

Enhancement of MR images using registration for signal averaging.

PURPOSE: With the advent of noninvasive neuroimaging, a plethora of digital human neuroanatomical atlases has been developed. The accuracy of these atlases is constrained by the resolution and signal-gathering powers of available imaging equipment. In an attempt to circumvent these limitations and to produce a high resolution in vivo human neuroanatomy, we investigated the usefulness of intrasubject registration for post hoc MR signal averaging. METHOD: Twenty-seven high resolution (7 x 0.78 and 20 x 1.0 mm3) T1-weighted volumes were acquired from a single subject, along with 12 double echo T2/proton density-weighted volumes. These volumes were automatically registered to a common stereotaxic space in which they were subsampled and intensity averaged. The resulting images were examined for anatomical quality and usefulness for other analytical techniques. RESULTS: The quality of the resulting image from the combination of as few as five T1 volumes was visibly enhanced. The signal-to-noise ratio was expected to increase as the root of the number of contributing scans to 5.2, n = 27. The improvement in the n = 27 average was great enough that fine anatomical details, such as thalamic subnuclei and the gray bridges between the caudate and putamen, became crisply defined. The gray/white matter boundaries were also enhanced, as was the visibility of any finer structure that was surrounded by tissue of varying T1 intensity. The T2 and proton density average images were also of higher quality than single scans, but the improvement was not as dramatic as that of the T1 volumes. CONCLUSION: Overall, the enhanced signal in the averaged images resulted in higher quality anatomical images, and the data lent themselves to several postprocessing techniques. The high quality of the enhanced images permits novel uses of the data and extends the possibilities for in vivo human neuroanatomy.

Artifacts↗

PubMed2004

Magnetic resonance evaluation of cerebral toxoplasmosis in patients with the acquired immunodeficiency syndrome.

PURPOSE: To evaluate and delineate the characteristics of cerebral toxoplasmosis lesions using a combination of magnetic resonance (MR) spectroscopy, diffusion, and perfusion studies. MATERIAL AND METHODS: A total of 8 patients with 23 lesions were evaluated on a 1.5-T MR system. Diffusion-weighted imaging (DWI) was performed with three 'b' values of 50, 500, and 1000 s/mm2, and the apparent diffusion coefficient maps were calculated. The diffusion-weighted appearances and the T2-weighted MR appearances of the lesions were compared. MR spectroscopy was performed using the point-resolved single-voxel technique with two TE values of 135 ms and 270 ms. Perfusion studies were carried out using the dynamic contrast-enhanced technique, and the relative cerebral blood volume maps were qualitatively and quantitatively analyzed. RESULTS: DWI revealed the majority of the lesions as having increased diffusion within their necrotic centers, with the ADC ranging from 0.5 to 3.01 (mean +/- SD: 1.49 +/- 0.7). All the lesions revealed a predominant lipid peak on MR spectroscopy and were extremely hypovascular on perfusion MR studies. CONCLUSION: MR diffusion, spectroscopy, and perfusion studies help in characterizing toxoplasmosis lesions and, in most cases, can be used in combination to help establish the diagnosis of toxoplasmosis.

AIDS-Related Opportunistic Infections↗

PubMed2005

Differential enhancing effects of alpha2,8-sialyltransferase on the cell proliferation and mobility.

alpha2,8-Sialyltransferase (alpha2,8S-T, GD3 synthase) has been reported to be involved in the enhanced cell proliferation of malignant tumors. Using a cloned cDNA of alpha2,8S-T, transfectant cells were established and the effects of the gene expression on the cell phenotypes were analyzed. In contrast with PC12 cells, in which we reported marked growth enhancement based on the transfection of alpha2,8S-T, Swiss3T3 cells showed no enhancement in either cell proliferation or phosphorylation of MAP kinases after the transfection of alpha2,8S-T when treated with platelet-derived growth factor. Correspondingly, the receptor for platelet-derived growth factor also showed no increased phosphorylation upon the factor stimulation. However, in the wound-healing scratching assay, the Swiss3T3 transfectant cells demonstrated increased mobility as the PC12 transfectant cells. These results suggest that the enhancing effects of alpha2,8S-T on the proliferation and mobility are differential depending on the cell types, and ganglioside-associating molecules in the individual cell types need to be investigated.

Animals↗

PubMed2006

Human myocardium: single-breath-hold MR T1 mapping with high spatial resolution--reproducibility study.

A prospective study approved by the local ethics committee was performed to establish the normal range and reproducibility of myocardial T1 values as assessed with single-breath-hold T1 mapping with high spatial resolution. With a 1.5-T magnetic resonance (MR) imaging system, baseline and contrast material-enhanced modified Look-Locker inversion recovery, or MOLLI, imaging was performed in 15 healthy volunteers who had given written informed consent. Image quality scores and myocardial T1 values were derived for standard short-axis segments and sections. Results were compared with those from a second MR imaging study performed on the same day (baseline only) and those from a third study performed on a different day (baseline and contrast enhanced; eight volunteers). Intra- and interobserver agreement were determined. Myocardial T1 maps were obtained rapidly in a reproducible fashion. A normal range for baseline and postcontrast myocardial T1 was established (baseline mean T1 in short-axis sections, 980 msec +/- 53 [standard deviation]; 95% confidence interval: 964, 997; number of sections, 43). This technique could enable direct quantification of changes in tissue characteristics in ischemic and inflammatory myocardial diseases.

Adult↗