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L Neckers

Publications and source records attributed to L Neckers.

61 records · Page 4Linked to original sources

Mononuclear cell-surface antigens during storage of banked blood.

The surface antigens present on lymphocyte subpopulations and monocytes in whole blood stored under standard blood bank conditions were analyzed with a series of monoclonal antibodies and a fluorescence-activated cell sorter. During the first week of storage, the percentage of viable cells bearing T lymphocyte markers declined from 66% to 29% (P less than 0.001). Within the T cell subset, there was a disproportionate decrease in the percentage of cells reacting with anti-Leu 3a (a helper T cell marker) resulting in a reduction in the measured ratio of helper-to-suppressor T cells (P less than 0.01). The relative percentage of cells bearing B lymphocyte markers increased from 11% to 31% (P less than 0.001). The proportion of HLA-DR-positive cells that were B cells increased during the first week of storage from 38% to 65% (P less than 0.01). The degree of residual antigen expression as measured by the remaining median intensity of fluorescence was significantly greater for B cell and HLA-DR antigens as compared with T cell antigens. The measured changes during storage in the relative proportions of mononuclear cells expressing cell-surface antigens probably result from a combination of differential residual antigen expression and differential survival of mononuclear subpopulations. The presence of adenine in the anticoagulant-preservative solution had no measurable effect. Storage at 4 C, however, was shown to result in a 70% decrease in the proportion of antigen-bearing T cells, even as early as 24 hr of storage. The findings may have bearing on the beneficial effect of blood transfusion in renal transplant recipients, as well as on experimental models of the immune response to transfusion.

Adenine↗

Regulation of 5-hydroxytryptamine metabolism in mouse brain by adrenal glucocorticoids.

The effects of glucocorticoid hormone on the metabolism of brain 5-hydroxytryptamine (5-HT) were studied in mice. A single injection of hydrocortisone acetate (HCA; 20 mg/kg, i.p.) accelerated the accumulation of 5-HT in whole brain after inhibition of monoamine oxidase activity by paragyline. The hormone did not appear to change brain tryptophan hydroxylase or 5-hydroxytryptophan decarboxylase activity. However, tryptophan levels in brain were elevated by 50% within 1 h after treatment with HCA. The effect of HCA on brain tryptophan levels was localized mainly in the nerve endings. In vitro synaptosomal preparations, HCA at 10(-5)-10(-7)M or corticosterone at 10(-5) M was found to stimulate the uptake of L-[3H]-tryptophan by the synaptosomes while androgenic and progesterone-like steroids were ineffective. These results demonstrate that glucocorticoids may directly act on nerve terminals in the regulation of 5-HT synthesis through an action on the uptake of tryptophan.

5-Hydroxytryptophan↗

Prostaglandin E2 and vasoactive intestinal peptide increase vascular endothelial cell growth factor mRNAs in lung cancer cells.

The effects of prostaglandin E2 (PGE2) and vasoactive intestinal peptide (VIP) on vascular endothelial cell growth factor (VEGF) mRNAs were investigated using lung cancer cells. By RT-PCR, VEGF(121), VEGF(165), and VEGF(189), but not VEGF(206) isoforms were detected in all lung cancer cell lines and biopsy specimens examined. By Northern blot, VEGF mRNA was detected in all small cell lung cancer (SCLC) and non-SCLC (NSCLC) cell lines examined. PGE2, VIP and forskolin caused increased VEGF expression in a time- and concentration-dependent manner using NSCLC cell line NCI-H157. Approximately 1 microM PGE2, 0.1 microM VIP and 50 microM forskolin caused cAMP elevation, 64-, 33- and 128-fold, respectively, using NCI-H157 cells after 5 min. The increase in cAMP caused by PGE(2) and VIP was reversed by somatostatin (SST). Also 1 microM PGE2, 0.1 microM VIP and 50 microM forskolin increased the VEGF mRNA 2.0-, 1.5- and 2.3-fold, respectively, after 4 h. The increase in VEGF mRNA caused by PGE2, VIP and forskolin was inhibited by H-89, a protein kinase A inhibitor. A VIP receptor antagonist, VIPhybrid, inhibited the increase in cAMP and VEGF mRNA caused by VIP. By ELISA, VEGF was detected in the conditioned media exposed to the lung cancer cell lines. These results suggest that VEGF synthesis in and secretion from lung cancer cells can be regulated by agents, which cause adenylyl cyclase activation.

Adenylyl Cyclases↗