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  • Progesterone modulates brain-derived neurotrophic factor and choline acetyltransferase in degenerating Wobbler motoneurons. 17052708

    Progesterone (PROG) shows neuroprotective effects in nervous system diseases. The Wobbler mouse, a model of motoneuron degeneration, suffers a mutation of the Vsp154 gene on chromosome 11 leading to motoneuron vacuolation and astrocytosis of the spinal cord. Previous work has demonstrated beneficial effects of PROG in the Wobbler mouse. As an extension of this work, we now studied steroid effects on neuronal brain-derived neurotrophic factor (BDNF) mRNA and protein, on choline acetyltransferase (ChAT) immunoreactivity (IR) and activity in the spinal cord, and on recovery of muscle atrophy. Wobbler mice received implants of PROG pellets (20 mg) at 6 and 10 weeks of age and were killed at 14 weeks. In situ hybridization for BDNF mRNA demonstrated that grain density in large (>600 microm2) and medium size (600 microm2) ventral horn neurons was decreased in untreated Wobblers, whereas PROG treatment increased BDNF mRNA in both neuronal types. PROG also induced a subcellular redistribution of BDNF protein, which in controls and steroid-naive Wobblers showed a predominant perinuclear and nucleolar location, whereas after PROG treatment, it was detected in cytoplasmic aggregates. ChAT activity was reduced by 55.3% in muscles of untreated Wobbler mice, whereas a significant increment was obtained after PROG treatment. Wobblers also showed reduced number of ChAT positive motoneurons, but this number was restored to normal by PROG. Finally, the pronounced biceps atrophy of steroid-naive Wobbler mice was slightly but significantly increased by PROG-treatment. Considering the important role played by neurotrophins on neuronal function, changes in BDNF might be part of the PROG activated-pathways to provide neuroprotection and re-establish neurotransmission and neuromuscular function in this degeneration model.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB143
    Nombre del producto:
    Anti-Choline Acetyltransferase (ChAT) Antibody

  • Effects of carrageenan and morphine on acute inflammation and pain in Lewis and Fischer rats. 16603335

    The present study used inbred, histocompatible Fischer 344 (FIS) and Lewis (LEW) rats to begin to explore the role of the hypothalamic-pituitary-adrenal (HPA) axis in the immune processes and pain behavior associated with the carrageenan model of acute hindpaw inflammation. Because the HPA axis contributes in part to morphine's analgesic and immunomodulatory properties, the present study also assessed the effects of morphine in carrageenan-inflamed LEW and FIS rats. The results showed that carrageenan-induced hindpaw swelling and pain behavior were greater in FIS than in LEW rats. The enhanced hindpaw swelling in FIS rats correlated with an increase in myeloperoxidase (MPO; a measure of neutrophils) in the inflamed hindpaw. FIS rats showed lower circulating levels of TNFalpha, higher IL-6 levels, and similar IL-1beta and nitric oxide levels, when compared to LEW rats. Morphine produced a significant decrease in carrageenan-induced hindpaw swelling and MPO in both strains, but morphine did not significantly alter circulating cytokine/mediator levels. Morphine's analgesic effects were greater in the inflamed than the noninflamed hindpaw, and they did not correlate with morphine's anti-inflammatory effects. In fact, low doses of morphine produced a mechanical allodynia and hyperalgesia in the noninflamed hindpaw of FIS, but not LEW, rats. These results suggest a positive relationship between HPA axis activity and acute inflammation and inflammatory pain. In contrast, little evidence is provided for HPA axis involvement in morphine's anti-inflammatory or analgesic effects.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AP307P
    Nombre del producto:
    Goat Anti-Rabbit IgG Antibody, (H+L) HRP conjugate

  • Erythrophagocytosis by angiogenic endothelial cells is enhanced by loss of erythrocyte deformability. 20146933

    OBJECTIVE: Angiogenic endothelial cells can function as phagocytes, and phagocytosis is initiated via the opsonin lactadherin. In this study, we examined the interaction between lactadherin-opsonized erythrocytes with reduced deformability and angiogenic endothelium, as loss of deformability is characteristic for suicidal and aged erythrocytes. MATERIALS AND METHODS: We used the Arg-Gly-Asp (RGD)-modified erythrocyte model and investigated the deformability parameter by cross-linking erythrocyte membranes through treatment with glutaraldehyde. Association in vitro with primary endothelial cells was detected by flow cytometry and visualized by light, fluorescent, and electron microscopy. Involvement of two crucial factors in phagocytosis, alpha(v)-integrins and Rho guanosine triphosphatase family member Rac1, was studied using small interfering RNA technology. Modified erythrocytes were administered in vivo into tumor-bearing mice to detect phagocytosis by endothelial cells. RESULTS: Glutaraldehyde-treated (rigid) RGD-modified erythrocytes showed a strongly enhanced endothelial cell association compared to flexible RGD-modified erythrocytes. Knockdown by small interfering RNA lipoplexes of alpha(v)-integrins and Rac1 confirmed classical tethering and internalization of rigid RGD-erythrocytes. Upon in vivo administration, tumor endothelium showed pronounced erythrophagocytosis. CONCLUSION: The pronounced phagocytosis of opsonized erythrocytes with reduced deformability by angiogenic growth factor-activated endothelial cells evokes new insights in endothelial cell function and suggests a role for these endothelial cells in (hematological) disorders because of their capacity to clear disordered erythrocytes.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB1930
    Nombre del producto:
    Anti-Integrin alphaV Antibody, CT, Intracellular

  • The presence of active Cdk5 associated with p35 in astrocytes and its important role in process elongation of scratched astrocyte. 17295212

    Cyclin-dependent kinase 5 (Cdk5) is a unique member of the Cdk family; its kinase activity requires association with its activator, p35 or p39. p35 is the strongest and best characterized activator. Previous studies showed that p35 is a neuron-specific protein that restricts Cdk5 activity in neurons. However, a high expression level of Cdk5 is found in astrocytes, which raises the possibility that astrocytic Cdk5 is functional. Here we show the presence of functional Cdk5 associated with p35 in astrocytes and demonstrate its important role in process elongation of scratched astrocytes. We found that p35 and glial fibrillary acidic protein (GFAP) were co-localized in primary cultured and acute isolated brain cells. Cdk5 could form an immunocomplex with p35 and its activity was shown in pure primary cultured astrocytes. p35 was upregulated in astrocytes injured by scratching, concomitantly with upregulation of Cdk5 kinase activity. Pretreatment of the scratched astrocytes with a Cdk5 inhibitor, roscovitine, could delay wound healing by inhibiting the reorganization of tubulin, GFAP, and the extension of hypertrophic processes. Moreover, overexpression of dominant negative Cdk5 could shorten the length of extending protrusion of reactive astrocytes. Thus, our findings demonstrated that functional Cdk5, associated with p35, was expressed in astrocytes and its activity could be upregulated in reactive astrocytes, a new role of Cdk5 that has never been reported in the nervous system. The present study may provide new insight for understanding the multifunctional protein complex Cdk5/p35 in the nervous system.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-364
    Nombre del producto:
    Anti-Cdk5 Antibody, clone DC17

  • Disease Modeling Using Embryonic Stem Cells: MeCP2 Regulates Nuclear Size and RNA Synthesis in Neurons. 22865604

    Mutations in the gene encoding the methyl-CpG-binding protein MECP2 are the major cause of Rett syndrome, an autism spectrum disorder mainly affecting young females. MeCP2 is an abundant chromatin-associated protein, but how and when its absence begins to alter brain function is still far from clear. Using a stem cell-based system allowing the synchronous differentiation of neuronal progenitors, we found that in the absence of MeCP2, the size of neuronal nuclei fails to increase at normal rates during differentiation. This is accompanied by a marked decrease in the rate of ribonucleotide incorporation, indicating an early role of MeCP2 in regulating total gene transcription, not restricted to selected mRNAs. We also found that the levels of brain-derived neurotrophic factor (BDNF) were decreased in mutant neurons, while those of the presynaptic protein synaptophysin increased at similar rates in wild-type and mutant neurons. By contrast, nuclear size, transcription rates, and BDNF levels remained unchanged in astrocytes lacking MeCP2. Re-expressing MeCP2 in mutant neurons rescued the nuclear size phenotype as well as BDNF levels. These results reveal a new role of MeCP2 in regulating overall RNA synthesis in neurons during the course of their maturation, in line with recent findings indicating a reduced nucleolar size in neurons of the developing brain of mice lacking Mecp2. STEM Cells2012;30:2128-2139.
    Tipo de documento:
    Referencia
    Referencia del producto:
    07-013
    Nombre del producto:
    Anti-MeCP2 Antibody

  • Atorvastatin inhibits ABCA1 expression and cholesterol efflux in THP-1 macrophages by an LXR-dependent pathway. 18427282

    The effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and cholesterol efflux remains controversial. In an effort to clarify this issue, ABCA1 expression and apolipoprotein AI (apoAI)-mediated cholesterol efflux after atorvastatin treatment were investigated in THP-1 macrophages. Atorvastatin from 2 microM to 40 microM dose-dependently inhibited ABCA1 expression in human monocyte-derived macrophages and phorbol 12-myristate 13-acetate (PMA)-stimulated THP-1 monocytes. ApoAI-mediated cholesterol efflux was reduced in PMA-stimulated THP-1 cells treated with atorvastatin, this effect was abolished with acetylated low-density lipoprotein (LDL) pretreatment. Atorvastatin treatment also dose-dependently reduced liver X receptor alpha (LXRalpha) expression and Rho activation. Rho activation by farnysylpyophosphate (FPP) and lysophosphatidic acid (LPA) did not salvage, but further depressed, the cholesterol efflux and ABCA1 expression in the presence of atorvastatin. Without atorvastatin, Rho activation by mevalonate, FPP, and LPA diminished apoAI-mediated cholesterol efflux, and Rho activation by GTPgammaS also decreased ABCA1 messenger ribonucleic acid (mRNA) by 16%. Furthermore, Rho inhibition by C3 exoenzyme increased ABCA1 mRNA by 48% despite a 17% decrease in apoAI-mediated cholesterol efflux. LXRalpha agonists (T01901317 and 22(R)-hydroxycholesterol) prevented any reductions in cholesterol efflux or ABCA1 expression associated with atorvastatin treatment. Furthermore, Western blot analysis demonstrated the reciprocal inhibition of Rho and LXRalpha. In conclusion, atorvastatin decreases ABCA1 expression in noncholesterol-loaded macrophages in an LXRalpha- but not Rho-dependent pathway; this effect can be compromised after acetylated LDL cholesterol loading.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-778
    Nombre del producto:
    Anti-Rho (-A Antibody, -B, -C), clone 55

  • Altered patterning of dentate granule cell mossy fiber inputs onto CA3 pyramidal cells in limbic epilepsy. 20014385

    Impaired gating by hippocampal dentate granule cells may promote the development of limbic epilepsy by facilitating seizure spread through the hippocampal trisynaptic circuit. The second synapse in this circuit, the dentate granule cell≫CA3 pyramidal cell connection, may be of particular importance because pathological changes occurring within the dentate likely exert their principal effect on downstream CA3 pyramids. Here, we utilized GFP-expressing mice and immunolabeling for the zinc transporter ZnT-3 to reveal the pre- and postsynaptic components of granule cell≫CA3 pyramidal cell synapses following pilocarpine-epileptogenesis. Confocal analyses of these terminals revealed that while granule cell presynaptic giant boutons increased in size and complexity 1 month after status epilepticus, individual thorns making up the postsynaptic thorny excrescences of the CA3 pyramidal cells were reduced in number. This reduction, however, was transient, and 3 months after status, thorn density recovered. This recovery was accompanied by a significant change in the distribution of thorns along pyramidal cells dendrites. While thorns in control animals tended to be tightly clustered, thorns in epileptic animals were more evenly distributed. Computational modeling of thorn distributions predicted an increase in the number of boutons required to cover equivalent numbers of thorns in epileptic vs. control mice. Confirming this prediction, ZnT-3 labeling of presynaptic giant boutons apposed to GFP-expressing thorns revealed a near doubling in bouton density, while the number of individual thorns per bouton was reduced by half. Together, these data provide clear evidence of novel plastic changes occurring within the epileptic hippocampus.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB3080
    Nombre del producto:
    Anti-Green Fluorescent Protein Antibody

  • Syndrome of inappropriate antidiuretic hormone secretion in patients with olfactory neuroblastoma. 22368044

    The syndrome of inappropriate antidiuretic hormone secretion (SIADH) has been reported as a paraneoplastic syndrome in many different types of malignancies. Several case reports of SIADH have been reported in patients with olfactory neuroblastoma (ONB), but the exact incidence is unknown. The purpose of this study was to review our experience with olfactory neuroblastoma and to identify all patients who had a history of SIADH prior to the diagnosis of ONB.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB1565
    Nombre del producto:
    Anti-Vasopressin Antibody

  • Effects of the integrin-linked kinase inhibitor QLT0267 on squamous cell carcinoma of the head and neck. 17224516

    To study the expression of integrin-linked kinase (ILK) in human squamous cell carcinoma of the head and neck (SCCHN) tumor specimens and cell lines and the efficacy of the novel small molecule QLT0267.Immunohistochemical analysis of 17 SCCHN tumor tissue specimens and 3 normal tongue tissue specimens for ILK expression and in vitro analysis of the effectiveness of QLT0267 on SCCHN cells.Academic medical center.Expression levels of ILK in SCCHN tumor specimens and cell lines and the efficacy of QLT0267 in inhibiting cell growth and inducing apoptosis in SCCHN cell lines.Most SCCHN tumor specimens stained for ILK, whereas none of the 3 normal tongue tissue specimens stained for ILK. Integrin-linked kinase was expressed in all 6 SCCHN cell lines tested. In 4 pairs of normal and SCCHN tumor specimens, ILK expression and activity were higher in most tumor samples tested. A kinase assay showed that QLT0267 inhibited the ILK activity of 2 SCCHN cell lines (TU167 and MDA1986). Modified tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, DNA fragmentation ladder, and TUNEL (terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridine triphosphate nick-end()labeling) assays showed that QLT0267 inhibited cell growth and induced apoptosis in these 2 cell lines. A dose-dependent decrease in Akt phosphorylation was observed for these 2 cell lines on treatment with QLT0267.Integrin-linked kinase is overexpressed in SCCHN tumor specimens. Targeting ILK with the small-molecule ILK inhibitor QLT0267 inhibits cell growth and induces apoptosis in SCCHN cell lines by reducing ILK activity and Akt phosphorylation. Integrin-linked kinase may be an attractive target for molecular therapy with which to enhance treatment of SCCHN.
    Tipo de documento:
    Referencia
    Referencia del producto:
    06-559

  • The C-terminus of Apc does not influence intestinal adenoma development or progression. 22009253

    Adenomatous polyposis coli (APC ) mutations are found in most colorectal tumours. These mutations are almost always protein-truncating, deleting both central domains that regulate Wnt signalling and C-terminal domains that interact with the cytoskeleton. The importance of Wnt dysregulation for colorectal tumourigenesis is well characterized. It is, however, unclear whether loss of C-terminal functions contributes to tumourigenesis, although this protein region has been implicated in cellular processes--including polarity, migration, mitosis, and chromosomal instability (CIN)—that have been postulated as critical for the development and progression of intestinal tumours. Since almost all APC mutations in human patients disrupt both central and C-terminal regions, we created a mouse model to test the role of the C-terminus of APC in intestinal tumourigenesis. This mouse (Apc(ΔSAMP)) carries an internal deletion within Apc that dysregulates Wnt by removing the beta-catenin-binding and SAMP repeats, but leaves the C-terminus intact. We compared Apc(ΔSAMP) mice with Apc(1322T) animals. The latter allele represented the most commonly found human APC mutation and was identical to Apc(ΔSAMP) except for absence of the entire C-terminus. Apc(ΔSAMP) mice developed numerous intestinal adenomas indistinguishable in number, location, and dysplasia from those seen in Apc(1322T) mice. No carcinomas were found in Apc(ΔSAMP) or Apc(1322T) animals. While similar disruption of the Wnt signalling pathway was observed in tumours from both mice, no evidence of differential C-terminus functions (such as cell migration, CIN, or localization of APC and EB1) was seen. We conclude that the C-terminus of APC does not influence intestinal adenoma development or progression.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB5977
    Nombre del producto:
    Anti-Musashi-1 Antibody