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  • Mitochondrial prohibitins and septin 9 are implicated in the onset of rat hepatocarcinogenesis. 20935162

    In the present study, protein lysates from microdissected glutathione S-transferase placental-form-positive (GST-P(+)) foci and hepatocellular carcinomas from livers of rats treated with N-diethylnitrosamine followed by phenobarbital at doses of 0 and 500 ppm in the diet for 10 and 33 weeks were analyzed using QSTAR Elite liquid chromatography with tandem mass spectrometry and iTRAQ technology. Among 75 proteins, a total of 27 and 50 proteins displaying significant quantitative changes comparing with adjacent normal-appearing liver tissue were identified in GST-P(+) foci of initiation control and promotion groups, respectively, which are related to transcription, protein folding, cytoskeleton filaments reorganization, cell cycle control, nuclear factor (erythroid-derived 2)-like 2 (NRF2)-mediated oxidative stress responses, lipid metabolism, glutathione metabolism, oxidative phosphorylation, and signal transduction. Furthermore, Ingenuity Pathway and bioinformatic analyses revealed that expression changes of genes encoding proteins with altered expression detected in GST-P(+) foci are likely to be controlled by c-myc, NRF2, aryl hydrocarbon receptor, nuclear factor kappa B, and hepatocyte nuclear factor 4 transcriptional factors. Coordinated overexpression of mitochondrial chaperons prohibitin (PHB) and prohibitin 2 (PHB2), septin 9 (SEPT9), neurabin 1, and other cytoskeletal and functional proteins in areas of GST-P(+) foci during initiation and/or promotion stages of rat hepatocarcinogenesis was associated with induction of cell proliferation and might be responsible for the neoplastic transformation of rat liver preneoplastic lesions. Newly discovered elevation of PHB, PHB2, and SEPT9 in GST-P(+) foci and tumors, imply that they might play important role in the onset of liver cancer and be of potential values in the studies of hepatocarcinogenesis.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Triptolide induces cell-cycle arrest and apoptosis of human multiple myeloma cells in vitro via altering expression of histone demethylase LSD1 and JMJD2B. 22120968

    To elucidate the relationship between triptolide-induced changes in histone methylation and its antitumor effect on human multiple myeloma (MM) cells in vitro.Human multiple myeloma cell line RPMI8226 was used. Apoptosis was evaluated using Annexin-V-FITC/PI-labeled flow cytometry, Hoechst 33258 staining, and transmission electron microscopy. Flow cytometry was used to detect the cell cycle distribution of the apoptotic cells. The presence of the LSD1, JMJD2B, H3K4me2, H3K9me2, and H3K36me2 proteins was verified by Western blot analysis. Semi-quantitative real-time PCR was performed to examine the expression of LSD1 and JMJD2B.Triptolide (10-160 nmol/L) suppressed the proliferation of MM cells in a dose- and time-dependent manner with an IC(50) value of 99.2 ± 9.0 nmol/L at 24 h. Triptolide (50 nmol/L) induced G(0)/G(1) cell cycle arrest in MM cells. The agent (50-150 nmol/L) induced apoptosis of MM cells in a dose-dependent manner. The same concentrations of triptolide suppressed the expression of dimethylated H3K4, dimethylated H3K9 and dimethylated H3K36 by altering the expression of histone demethylase LSD1 and JMJD2B without affecting the expression of histone demethylase LSD1.Triptolide potently inhibits the growth of MM cells via regulating the expression of histone demethylase LSD1 and JMJD2B, which lead to abnormal histone methylation.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Chimeric L1-L2 virus-like particles as potential broad-spectrum human papillomavirus vaccines. 19640991

    The amino (N) terminus of the human papillomavirus (HPV) minor capsid protein L2 can induce low-titer, cross-neutralizing antibodies. The aim of this study was to improve immunogenicity of L2 peptides by surface display on highly ordered, self-assembled virus-like particles (VLP) of major capsid protein L1, and to more completely characterize neutralization epitopes of L2. Overlapping peptides comprising amino acids (aa) 2 to 22 (hereafter, chimera or peptide 2-22), 13 to 107, 18 to 31, 17 to 36, 35 to 75, 75 to 112, 115 to 154, 149 to 175, and 172 to 200 of HPV type 16 (HPV16) L2 were genetically engineered into the DE surface loop of bovine papillomavirus type 1 L1 VLP. Except for chimeras 35-75 and 13-107, recombinant fusion proteins assembled into VLP. Vaccination of rabbits with Freund's adjuvanted native VLP induced higher L2-specific antibody titers than vaccination with corresponding sodium dodecyl sulfate-denatured proteins. Immune sera to epitopes within residues 13 to 154 neutralized HPV16 in pseudovirion neutralization assays, whereas chimera 17-36 induced additional cross-neutralization to divergent high-risk HPV18, -31, -45, -52, and -58; low-risk HPV11; and beta-type HPV5 (titers of 50 to 10,000). Aluminum hydroxide-monophosphoryl lipid A (Alum-MPL)-adjuvanted VLP induced similar patterns of neutralization in both rabbits and mice, albeit with 100-fold-lower titers than Freund's adjuvant. Importantly, Alum-MPL-adjuvanted immunization with chimeric HPV16L1-HPV16L2 (peptide 17-36) VLP induced neutralization or cross-neutralization of HPV16, -18, -31, -45, -52, and -58; HPV6 and -11; and HPV5 (titers of 50 to 100,000). Immunization with HPV16 L1-HPV16 L2 (chimera 17-36) VLP in adjuvant applicable for human use induces broad-spectrum neutralizing antibodies against HPV types evolutionarily divergent to HPV16 and thus may protect against infection with mucosal high-risk, low-risk, and beta HPV types and associated disease.
    Document Type:
    Reference
    Product Catalog Number:
    13-107
    Product Catalog Name:
    Core Histones

  • Dissociated secondary hyperalgesia in a subject with a large-fibre sensory neuropathy. 8393170

    In the skin surrounding a site of injury, hyperalgesia develops to mechanical stimuli. Two types of secondary hyperalgesia (to light touch and punctate stimuli) have recently been differentiated, based on different durations and sizes of the area involved. We studied secondary hyperalgesia in a subject who had a loss of myelinated afferent nerve fibres below the neck that spared the A delta group. Stroking with a cotton swab was not perceived anywhere on affected skin either before or after injection of 60 micrograms of capsaicin. Thus, there was no hyperalgesia to light touch. Capsaicin injection into the volar forearm evoked normal pain and flare. A von Frey probe exerting a force of 40 mN was perceived as sharp. The sensation of sharpness was more pronounced up to 2 cm outside the flare zone for at least 16 min following the injection (tested with a 200 mN von Frey probe). Thus, hyperalgesia to punctate stimuli developed as in healthy subjects. These data support the model that hyperalgesia to light touch (allodynia) is due to sensitisation of central pain-signaling neurones to low-threshold mechanoreceptor input (A beta fibres). In contrast, punctate hyperalgesia is likely to be due to sensitisation to nociceptor input (A delta or C fibres).
    Document Type:
    Reference
    Product Catalog Number:
    20-119

  • Matrix metalloproteinase inhibition attenuates left ventricular remodeling and dysfunction in a rat model of progressive heart failure. 11342481

    BACKGROUND: Matrix metalloproteinase (MMP) activation contributes to tissue remodeling in several disease states, and increased MMP activity has been observed in left ventricular (LV) failure. The present study tested the hypothesis that MMP inhibition would influence LV remodeling and function in developing LV failure. METHODS AND RESULTS: LV size and function were measured in 5 groups of rats: (1) obese male spontaneously hypertensive heart failure rats (SHHF) at 9 months (n=10), (2) SHHF at 13 months (n=12), (3) SHHF rats treated with an MMP inhibitor during months 9 to 13 (PD166793 5 mg. kg(-1). d(-1) PO; n=14), (4) normotensive Wistar-Furth rats (WF) at 9 months (n=12), and (5) WF at 13 months (n=12). Plasma concentrations of the MMP inhibitor (116+/-11 micromol/L) reduced in vitro LV myocardial MMP-2 activity by approximately 100%. LV function and geometry were similar in WF rats at 9 and 13 months. LV peak +dP/dt was unchanged at 9 months in SHHF but by 13 months was reduced in the SHHF group compared with WF (3578+/-477 versus 5983+/-109 mm Hg/s, P/=0.05). LV volume measured at an equivalent ex vivo pressure (10 mm Hg) was increased in SHHF at 9 months compared with WF (443+/-12 versus 563+/-33 mL, P/=0.05) and increased further by 13 months (899+/-64 mL, P/=0.05). LV myocardial MMP-2 activity was increased by approximately 2-fold in SHHF at 9 and 13 months. With MMP inhibition, LV peak +dP/dt was similar to WF values and LV volume was reduced compared with untreated SHHF values (678+/-28 mL, P/=0.05). CONCLUSIONS: MMP activity contributes to LV dilation and progression to LV dysfunction in a rodent HF model, and direct MMP inhibition can attenuate this process.
    Document Type:
    Reference
    Product Catalog Number:
    MAB3321
    Product Catalog Name:
    Anti-MMP-13 Antibody, clone 181-15A12

  • Apigenin Induces Apoptosis through Mitochondrial Dysfunction in U-2 OS Human Osteosarcoma Cells and Inhibits Osteosarcoma Xenograft Tumor Growth in Vivo. 23066961

    The cytostatic drug from natural products has acted as a chemotherapeutic agent used in treatment of a wide variety of cancers. Apigenin, a type of flavonoid, exhibits anticancer actions, but there is no report to show that apigenin induced apoptosis in osteosarcoma cells. The aim of this study was to investigate the effects of apigenin on U-2 OS human osteosarcoma cells and clarify that the apigenin-induced apoptosis-associated signals. The cytotoxic effects of apigenin were examined by culturing U-2 OS cells with or without apigenin. The percentage of viable cells via PI staining, apoptotic cells, productions of ROS and Ca(2+), and the level of mitochondrial membrane potential (ΔΨm) were assayed by flow cytometry. The levels of apoptosis-related proteins were measured by immunoblotting. Results indicated that apigenin significantly decreased cell viability. Apigenin effectively induced apoptosis through the activations of caspase-3, -8, -9, and BAX and promoted the release of AIF in U-2 OS cells. In nude mice bearing U-2 OS xenograft tumors, apigenin inhibited tumor growth. In conclusion, apigenin has anticancer properties for induction of cell apoptosis in U-2 OS cells and suppresses the xenograft tumor growth. These findings offer novel information that apigenin possibly possesses anticancer activity in human osteosarcoma.
    Document Type:
    Reference
    Product Catalog Number:
    04-434

  • Thyroid hormone stimulates Na-K-ATPase activity and its plasma membrane insertion in rat alveolar epithelial cells. 12740220

    Na-K-ATPase protein is critical for maintaining cellular ion gradients and volume and for transepithelial ion transport in kidney and lung. Thyroid hormone, 3,3',5-triiodo-l-thyronine (T3), given for 2 days to adult rats, increases alveolar fluid resorption by 65%, but the mechanism is undefined. We tested the hypothesis that T3 stimulates Na-K-ATPase in adult rat alveolar epithelial cells (AEC), including primary rat alveolar type II (ATII) cells, and determined mechanisms of the T3 effect on the Na-KATPase enzyme using two adult rat AEC cell lines (MP48 and RLE-6TN). T3 at 10-8 and 10-5 M increased significantly hydrolytic activity of Na-K-ATPase in primary ATII cells and both AEC cell lines. The increased activity was dose dependent in the cell lines (10-9-10-4 M) and was detected within 30 min and peaked at 6 h. Maximal increases in Na-K-ATPase activity were twofold in MP48 and RLE-6TN cells at pharmacological T3 of 10-5 and 10-4 M, respectively, but increases were statistically significant at physiological T3 as low as 10-9 M. This effect was T3 specific, because reverse T3 (3,3',5'-triiodo-l-thyronine) at 10-9-10-4 M had no effect. The T3-induced increase in Na-K-ATPase hydrolytic activity was not blocked by actinomycin D. No significant change in mRNA and total cell protein levels of Na-K-ATPase were detected with 10-9-10-5 M T3 at 6 h. However, T3 increased cell surface expression of Na-K-ATPase alpha1- or beta1-subunit proteins by 1.7- and 2-fold, respectively, and increases in Na-K-ATPase activity and cell surface expression were abolished by brefeldin A. These data indicate that T3 specifically stimulates Na-K-ATPase activity in adult rat AEC. The upregulation involves translocation of Na-K-ATPase to plasma membrane, not increased gene transcription. These results suggest a novel nontranscriptional mechanism for regulation of Na-K-ATPase by thyroid hormone.
    Document Type:
    Reference
    Product Catalog Number:
    05-382
    Product Catalog Name:
    Anti-Na+/K+ ATPase β-1 Antibody, clone C464.8

  • Monoclonal antibody DOG1.1 shows higher sensitivity than KIT in the diagnosis of gastrointestinal stromal tumors, including unusual subtypes. 19011564

    Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in the gastrointestinal tract. Approximately 85% of GISTs harbor activating mutations in the KIT or platelet-derived growth factor receptor alpha (PDGFRA) gene and approximately 95% of GISTs are positive for KIT (CD117) by immunohistochemistry. Nevertheless, approximately 5% of GISTs lack KIT expression. Inhibition of KIT and PDGFRA by tyrosine kinase inhibitors has revolutionized the treatment of GISTs and demands accurate tumor classification. DOG1.1 is a recently described mouse monoclonal antibody reported to have superior sensitivity and specificity compared with KIT (CD117) and CD34. We evaluated this new antibody on a group of 81 GISTs obtained from 74 patients with special regard to KIT-negative GISTs (n=28), pediatric GISTs (n=11), and GISTs associated with neurofibromatosis type I (NF1) (n=16). Conventional GISTs (n=26) were also included. All conventional KIT-positive GISTs, all NF1-associated GISTs, and 9/11 pediatric GISTs expressed DOG1.1. DOG1.1 was expressed in 10/28 (36%) of KIT-negative tumors. The staining pattern was cytoplasmic and/or membranous. This study demonstrates that DOG1.1 is a sensitive immunohistochemical marker for GIST, comparable with KIT, with the additional benefit of detecting 36% of KIT-negative GISTs. DOG1.1 is also a sensitive marker for unusual GIST subgroups lacking KIT or PDGFRA mutations. In tumors that are negative for both KIT and DOG1.1, mutational screening may be required to confirm the diagnosis of GIST.
    Document Type:
    Reference
    Product Catalog Number:
    MABC36

  • T(3) increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3. 11287359

    Triiodothyronine (T(3)) increases O(2) and nutrient flux through mitochondria (Mito) of many tissues, but it is unclear whether ATP synthesis is increased, particularly in different types of skeletal muscle, because variable changes in uncoupling proteins (UCP) and enzymes have been reported. Thus Mito ATP production was measured in oxidative and glycolytic muscles, as well as in liver and heart, in rats administered T(3) for 14 days. Relative to saline-treated controls, T(3) rats had 80, 168, and 62% higher ATP production in soleus muscle, liver, and heart, respectively, as well as higher activities of citrate synthase (CS; 63, 90, 25%) and cytochrome c oxidase (COX; 119, 225, 52%) in the same tissues (all P < 0.01). In plantaris muscle of T(3) rats, CS was only slightly higher (17%, P < 0.05) than in controls, and ATP production and COX were unaffected. mRNA levels of COX I and III were 33 and 47% higher in soleus of T(3) rats (P < 0.01), but there were no differences in plantaris. In contrast, UCP2 and -3 mRNAs were 2.5- to 14-fold higher, and protein levels were 3- to 10-fold higher in both plantaris and soleus of the T(3) group. We conclude that T(3) increases oxidative enzymes and Mito ATP production and Mito-encoded transcripts in oxidative but not glycolytic rodent tissues. Despite large increases in UCP expression, ATP production was enhanced in oxidative tissues and maintained in glycolytic muscle of hyperthyroid rats.
    Document Type:
    Reference
    Product Catalog Number:
    AB3046
    Product Catalog Name:
    Anti-Uncoupling Protein 3 Antibody

  • Effect of overweight on gastrointestinal microbiology and immunology: correlation with blood biomarkers. 19930761

    A cross-sectional study was carried out in order to compare intestinal microbiological and immunological biomarkers with blood glucose and lipids, satiety-related hormones and inflammatory biomarkers characterising differences between obese and normal weight subjects. Faecal and blood samples were obtained from twenty obese subjects with an average BMI of 32.9 kg/m2 and twenty normal weight subjects with an average BMI of 23.3 kg/m2. Blood insulin, TAG and leptin were significantly elevated, whereas concentrations of HDL and ghrelin were significantly decreased in the obese subjects. Inflammatory status in the obese subjects was characterised by a trend for elevated blood C-reactive protein (CRP; P = 0.06) and IL-6 (P = 0.02). The faecal microbial composition differed between the groups; less sulphate-reducing bacteria (P = 0.05) and a trend for less Bacteroides (P = 0.07) were measured for overweight subjects. Furthermore, an inverse correlation was demonstrated between faecal Bacteroides levels and waist circumference (P = 0.05). The faecal microbial metabolites differed between the groups; increased concentrations of branched-chain fatty acids, phenolics, valeric acid, di- and hydroxy acids were described in the obese subjects. No differences between the measured intestinal inflammatory biomarkers were detected. However, systemic inflammation (CRP and IL-6) was correlated with the faecal concentrations of phenolics and lactic acid (P < 0.05 and 0.05, and P < 0.01 and 0.05, respectively). In summary, weight-related differences were observed both in the intestinal microbial composition and its activity. The role of intestinal signals, such as phenolics and lactic acid in the development of weight-related problems, needs to be studied further.
    Document Type:
    Reference
    Product Catalog Number:
    PYYT-66HK
    Product Catalog Name:
    Human PYY (Total) RIA