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  • Sodium Chloride Increases Aβ Levels by Suppressing Aβ Clearance in Cultured Cells. 26075716

    Recent studies suggest that high-salt diet is associated with cognitive decline in human and mouse. The fact that genetic factors account for less than 50% cases of sporadic Alzheimer's disease (AD) highlights the important contribution of environmental factors, such as high-salt diet, in AD pathogenesis. However, whether and how high-salt diet fits the "amyloid cascade" hypothesis remains unexplored. Here, we show sodium chloride (NaCl) could increase Aβ levels in the medium of HEK293 cells overexpressing amyloid precursor protein (APP) or C99 fragment. NaCl treatment dose not affect APP level, gamma secretase level or activity. Instead, NaCl treatment suppresses the capacity of cells to clear Aβ and reduces Apolipoprotein E (ApoE) level. Finally, NaCl treated THP-1 or BV2 cells are inefficient in clearing Aβ when co-cultured with rat primary neurons. Our study suggests that high-salt diet may increase AD risk by directly modulating Aβ levels.
    Document Type:
    Reference
    Product Catalog Number:
    MAB5232
    Product Catalog Name:
    Anti-Presenilin-1 Antibody, loop, a.a. 263-378, CT, clone PS1-loop

  • Stability of thiotepa (lyophilized) in 0.9% sodium chloride injection. 9397220

    The stability of thiotepa in a new formulation of the drug was studied. Vials of Thioplex (Immunex), a relatively new lyophilized formulation of thiotepa, were reconstituted with sterile water and diluted with 0.9% sodium chloride injection in polyvinyl chloride infusion bags to thiotepa concentrations of 0.5, 1, and 3 mg/mL. The solutions were stored at 8 and 25 degrees C in ambient light and analyzed at 0, 8, 24, and in most cases 48 hours for thiotepa concentration and chloro-adduct formation by stability-indicating high-performance liquid chromatography. Thiotepa 1 and 3 mg/mL was stable for 48 hours at 8 degrees C and for 24 hours at 25 degrees C. Thiotepa 0.5 mg/mL was not stable at either temperature. Storage at 8 degrees C slowed but did not prevent chloro-adduct formation and loss of potency. The pH tended to increase with time; turbidity remained low. Thiotepa (lyophilized) 1 and 3 mg/mL in 0.9% sodium chloride injection was stable for 48 hours at 8 degrees C and for 24 hours at 25 degrees C; the drug was unstable when diluted to 0.5 mg/mL and stored under the same conditions.
    Document Type:
    Reference
    Product Catalog Number:
    06-457

  • Phosphorylation regulates NCC stability and transporter activity in vivo. 23833262

    A T60M mutation in the thiazide-sensitive sodium chloride cotransporter (NCC) is common in patients with Gitelman's syndrome (GS). This mutation prevents Ste20-related proline and alanine-rich kinase (SPAK)/oxidative stress responsive kinase-1 (OSR1)-mediated phosphorylation of NCC and alters NCC transporter activity in vitro. Here, we examined the physiologic effects of NCC phosphorylation in vivo using a novel Ncc T58M (human T60M) knock-in mouse model. Ncc(T58M/T58M) mice exhibited typical features of GS with a blunted response to thiazide diuretics. Despite expressing normal levels of Ncc mRNA, these mice had lower levels of total Ncc and p-Ncc protein that did not change with a low-salt diet that increased p-Spak. In contrast to wild-type Ncc, which localized to the apical membrane of distal convoluted tubule cells, T58M Ncc localized primarily to the cytosolic region and caused an increase in late distal convoluted tubule volume. In MDCK cells, exogenous expression of phosphorylation-defective NCC mutants reduced total protein expression levels and membrane stability. Furthermore, our analysis found diminished total urine NCC excretion in a cohort of GS patients with homozygous NCC T60M mutations. When Wnk4(D561A/+) mice, a model of pseudohypoaldosteronism type II expressing an activated Spak/Osr1-Ncc, were crossed with Ncc(T58M/T58M) mice, total Ncc and p-Ncc protein levels decreased and the GS phenotype persisted over the hypertensive phenotype. Overall, these data suggest that SPAK-mediated phosphorylation of NCC at T60 regulates NCC stability and function, and defective phosphorylation at this residue corrects the phenotype of pseudohypoaldosteronism type II.
    Document Type:
    Reference
    Product Catalog Number:
    MAB374
    Product Catalog Name:
    Anti-Glyceraldehyde-3-Phosphate Dehydrogenase Antibody, clone 6C5

  • Hypotensive hemorrhage increases calcium uptake capacity and Bcl-XL content of liver mitochondria. 17224795

    We tested the hypothesis that the response of mitochondrial uptake of calcium and content of Bcl proteins to reversible hemorrhagic shock increases the vulnerability for hepatocellular death. Pentobarbital-anesthetized rats were bled to a mean arterial pressure of 30 to 40 mmHg for 1 h. A subset was then resuscitated (isotonic sodium chloride solution, three times shed volume). Liver mitochondria were isolated at the end of hemorrhage and 1.5 h after the onset of resuscitation. Resuscitation accelerated mitochondrial respiration in the presence of adenosine diphosphate (state 3) above control (P<0.01). The respiratory control ratio ([RCR] state 3/state 4) was calculated using the respiratory rate in the presence of carboxyatractyloside (state 4). The RCR was depressed at the end of hemorrhage and recovered completely in response to resuscitation (P<0.05). The mitochondrial capacity for calcium uptake increased at the end of hemorrhage and remained greater than control (P<0.01) after resuscitation when plasma ornithine carbamoyltransferase (an index of hepatocellular injury) was greater than control (P<0.05). At this time, the capacity for calcium uptake was correlated with plasma ornithine carbamoyltransferase (r=0.819, P<0.01). Mitochondrial content of Bcl-xL, an antiapoptotic protein, was increased at the end of hemorrhage (P<0.03) with no further change after resuscitation and no change in mitochondrial Bak, a proapoptotic protein. Thus, mitochondrial mechanisms are triggered early during reversible hypovolemia that may limit the intensity of intracellular calcium signaling and its potential to cause cellular injury and death.
    Document Type:
    Reference
    Product Catalog Number:
    06-536
    Product Catalog Name:
    Anti-Bak Antibody, NT

  • The progeny of Arabidopsis thaliana plants exposed to salt exhibit changes in DNA methylation, histone modifications and gene expression. 22291972

    Plants are able to acclimate to new growth conditions on a relatively short time-scale. Recently, we showed that the progeny of plants exposed to various abiotic stresses exhibited changes in genome stability, methylation patterns and stress tolerance. Here, we performed a more detailed analysis of methylation patterns in the progeny of Arabidopsis thaliana (Arabidopsis) plants exposed to 25 and 75 mM sodium chloride. We found that the majority of gene promoters exhibiting changes in methylation were hypermethylated, and this group was overrepresented by regulators of the chromatin structure. The analysis of DNA methylation at gene bodies showed that hypermethylation in the progeny of stressed plants was primarily due to changes in the 5' and 3' ends as well as in exons rather than introns. All but one hypermethylated gene tested had lower gene expression. The analysis of histone modifications in the promoters and coding sequences showed that hypermethylation and lower gene expression correlated with the enrichment of H3K9me2 and depletion of H3K9ac histones. Thus, our work demonstrated a high degree of correlation between changes in DNA methylation, histone modifications and gene expression in the progeny of salt-stressed plants.
    Document Type:
    Reference
    Product Catalog Number:
    17-658
    Product Catalog Name:
    ChIPAb+ Acetyl-Histone H3 (Lys9) Purified - ChIP Validated Antibody and Primer Set

  • SLC4A11 prevents osmotic imbalance leading to corneal endothelial dystrophy, deafness, and polyuria. 20185830

    Maintenance of ion concentration gradients is essential for the function of many organs, including the kidney, the cornea, and the inner ear. Ion concentrations and fluid content in the cornea are regulated by endothelial cells that separate the collagenous avascular corneal stroma from the anterior eye chamber. Failure to maintain correct ion concentrations leads to swelling and destruction of the cornea. In the inner ear, the stria vascularis is responsible for generating proper ion concentrations in the endolymph, which is essential for hearing. Mutations of SLC4A11 in humans lead to syndromes associated with corneal dystrophy and perceptive deafness. The molecular mechanisms underlying these symptoms are poorly understood, impeding therapeutic interventions. The ion transporter SLC4A11 mediates sodium-dependent transport of borate as well as flux of sodium and hydroxyl ions in vitro. Here, we show that SLC4A11 is expressed in the endothelial cells of the cornea where it prevents severe morphological changes of the cornea caused by increased sodium chloride concentrations in the stroma. In the inner ear, SLC4A11 is located in fibrocytes underlying the stria vascularis. Loss of SLC4A11 leads to morphological changes in the fibrocytes and deafness. We demonstrate that SLC4A11 is essential for the generation of the endocochlear potential but not for regulation of potassium concentrations in the endolymph. In the kidney, SLC4A11 is expressed in the thin descending limb of Henle loop. SLC4A11 is essential for urinary concentration, suggesting that SLC4A11 participates in the countercurrent multiplication that concentrates urine in the kidney medulla.
    Document Type:
    Reference
    Product Catalog Number:
    AB3500P
    Product Catalog Name:
    Anti-Anion Exchanger 1 Antibody

  • Temporal and spatial disparity in cFOS expression and dopamine phenotypic differentiation in the neonatal mouse olfactory bulb. 16944318

    The mammalian olfactory bulb (OB) is among the few regions in adult brain which generates interneurons. A subpopulation of these phenotypically diverse interneurons is dopaminergic (DA) periglomerular cells. Full phenotypic development as indicated by expression of tyrosine hydroxylase (TH), the first enzyme in DA biosynthesis, requires afferent activity or equivalent depolarizing conditions. To investigate the hypothesis that cFOS regulates TH expression, this study analyzed OB slice cultures obtained from neonatal transgenic mice expressing 9 kb of TH promoter directing expression of green fluorescent protein (TH/GFP). Cultures were depolarized with 50 mM potassium chloride (KCl), the calcium channel blocker, nifedipine (10 microM) with KCl, or an equimolar concentration of sodium chloride (NaCl). Depolarization increased cFOS expression 6-fold peaking at about 3 h. Staining decreased rapidly returning to control, NaCl, levels by 48 h post-stimulation when TH/GFP expression was highest. Nifedipine blocked the increase in TH and cFOS suggesting that similar signal transduction pathways mediate both responses.
    Document Type:
    Reference
    Product Catalog Number:
    AB16901
    Product Catalog Name:
    Anti-Green Fluorescent Protein Antibody

  • Genomic-derived markers for early detection of calcineurin inhibitor immunosuppressant-mediated nephrotoxicity. 21865292

    Calcineurin inhibitor (CI) therapy has been associated with chronic nephrotoxicity, which limits its long-term utility for suppression of allograft rejection. In order to understand the mechanisms of the toxicity, we analyzed gene expression changes that underlie the development of CI immunosuppressant-mediated nephrotoxicity in male Sprague-Dawley rats dosed daily with cyclosporine (CsA; 2.5 or 25 mg/kg/day), FK506 (0.6 or 6 mg/kg/day), or rapamycin (1 or 10 mg/kg/day) for 1, 7, 14, or 28 days. A significant increase in blood urea nitrogen was observed in animals treated with CsA (high) or FK506 (high) for 14 and 28 days. Histopathological examination revealed tubular basophilia and mineralization in animals given CsA (high) or FK506 (low and high). We identified a group of genes whose expression in rat kidney is correlated with CI-induced kidney injury. Among these genes are two genes, Slc12a3 and kidney-specific Wnk1 (KS-Wnk1), that are known to be involved in sodium transport in the distal nephrons and could potentially be involved in the mechanism of CI-induced nephrotoxicity. The downregulation of NCC (the Na-Cl cotransporter coded by Slc12a3) in rat kidney following CI treatment was confirmed by immunohistochemical staining, and the downregulation of KS-Wnk1 was confirmed by quantitative real-time-polymerase chain reaction (qRT-PCR). We hypothesize that decreased expression of Slc12a3 and KS-Wnk1 could alter the sodium chloride reabsorption in the distal tubules and contribute to the prolonged activation of the renin-angiotensin system, a demonstrated contributor to the development of CI-induced nephrotoxicity in both animal models and clinical settings. Therefore, if validated as biomarkers in humans, SLC12A3 and KS-WNK1 could potentially be useful in the early detection and reduction of CI-related nephrotoxicity in immunosuppressed transplant patients when monitoring the health of kidney xenographs in clinical practice.
    Document Type:
    Reference
    Product Catalog Number:
    AB3553
    Product Catalog Name:
    Anti-Thiazide-Sensitive NaCl Cotransporter Antibody