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  • Ligation of endothelial alpha v beta 3 integrin increases capillary hydraulic conductivity of rat lung. 7554109

    Complement-mediated pulmonary edema results from increases in lung capillary hydraulic conductivity (Lp), possibly by receptor-mediated mechanisms. We considered the Lp effects of vitronectin and the vitronectin-containing complement complex SC5b-9, which ligate the integrin alpha v beta 3. Vitronectin, SC5b-9, and SC5b-9-enriched zymosan-activated serum all rapidly increased Lp, as determined by the split-drop technique in single lung capillaries of rat lung. The Lp increases were inhibited by a monospecific (LM609) and a polyclonal (R838) antibody against the alpha v beta 3 integrin but not by an irrelevant monoclonal antibody isotype matched with LM609, by a monoclonal antibody against the alpha v beta 5 integrin, or by preimmune rabbit serum. Vitronectin monomers failed to increase Lp. The tyrosine kinase blockers genistein and methyl 2,5-dihydroxycinnamate caused significant concentration-dependent inhibitions of Lp increases due to vitronectin and zymosan-activated serum. By contrast, the protein kinase C blocker calphostin C had no major effect. We conclude that (1) multivalent ligation of the luminally located alpha v beta 3 integrin of lung capillary endothelium increases transcapillary liquid flux, and (2) the dominant signal transduction pathway for this effect occurs through tyrosine kinase activation.
    Document Type:
    Reference
    Product Catalog Number:
    MAB88917
    Product Catalog Name:
    Anti-Vitronectin Antibody, clone 8E6(LJ8)

  • Alpha-synuclein deficiency in the C57BL/6JOlaHsd strain does not modify disease progression in the ME7-model of prion disease. 19879926

    We previously detailed how intrahippocampal inoculation of C57BL/6J mice with murine modified scrapie (ME7) leads to chronic neurodegeneration (Cunningham C, Deacon R, Wells H, Boche D, Waters S, Diniz CP, Scott H, Rawlins JN, Perry VH (2003) Eur J Neurosci 17:2147-2155.). Our characterization of the ME7-model is based on inoculation of this murine modified scrapie agent into C57BL/6J mice from Harlan laboratories. This agent in the C57BL/6J host generates a disease that spans a 24-week time course. The hippocampal pathology shows progressive misfolded prion (PrP(Sc)) deposition, astrogliosis and leads to behavioural dysfunction underpinned by the early synaptic loss that precedes neuronal death. The Harlan C57BL/6J, although widely used as a wild type mouse, are a sub-strain harbouring a spontaneous deletion of alpha-synuclein with the full description C57BL/6JOlaHsd. Recently alpha-synuclein has been shown to ameliorate the synaptic loss in a mouse model lacking the synaptic chaperone CSP-alpha. This opens a potential confound of the ME7-model, particularly with respect to the signature synaptic loss that underpin the physiological and behavioural dysfunction. To investigate if this strain-selective loss of a candidate disease modifier impacts on signature ME7 pathology, we compared cohorts of C57BL/6JOlaHsd (alpha-synuclein negative) with the founder strain from Charles Rivers (C57BL/6JCrl, alpha-synuclein positive). There were subtle changes in behaviour when comparing control animals from the two sub-strains indicating potentially significant consequences for studies assuming neurobiogical identity of both strains. However, there was no evidence that the absence of alpha-synuclein modifies disease. Indeed, accumulation of PrP(Sc), synaptic loss and the behavioural dysfunction associated with the ME7-agent was the same in both genetic backgrounds. Our data suggest that alpha-synuclein deficiency does not contribute to the compartment specific processes that give rise to prion disease mediated synaptotoxicity and neurodegeneration.
    Document Type:
    Reference
    Product Catalog Number:
    MAB368

  • Identification of orexins and cognate receptors in the lacrimal gland of sheep. 22465661

    The aim of the present work was to study, by means of immunohistochemical and RT-PCR techniques, the presence and distribution of immunopositivity for orexin A and B (OXA and OXB) and orexin type 1 and 2 receptors (OX(1)R and OX(2)R) in the lacrimal gland of sheep as well as the gene expressions for prepro-orexin (PPOX) and cognate receptors. In serial sections, positive staining for OXA and OXB were localized in the same nervous fibers within the connective tissue septa. Positive staining for OX(1)R was evidenced in the wall of small arteries while that for OX(2)R was observed in the secretory portion of the acinar gland cells with a characteristic localization in the apical cytoplasm. RT-PCR analysis showed the presence of transcripts for PPOX, OX(1)R and OX(2)R in the sheep lacrimal gland; the gene expression of OX(1)R was two-fold greater (p<0.01) than that of OX(2)R. Taken together the present findings raise intriguing questions on the potential role of the orexinergic system in the regulation of lacrimal gland functions that require further investigations.
    Document Type:
    Reference
    Product Catalog Number:
    AP132B
    Product Catalog Name:
    Goat Anti-Rabbit IgG Antibody, biotin-SP conjugate