Preparation of highly labelled 3H-thyreotropin releasing hormone (PGA-HIS-PRO(NH(2))) by catalytic hydrogenolysis.
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Journal Article↗
Biomedical subjects
P Pradelles
Publications and source records attributed to P Pradelles.
Pharmacological modulation of interleukin 1 production by cultured endothelial cells from human umbilical veins.
Solid-phase enzyme immunoassays (with high-turnover acetylcholinesterase as label) for human IL-1 alpha and IL-1 beta were applied to quantify the production of these factors by cultured human umbilical vein endothelial cells (HUVECs). Immunoreactive IL-1s exhibited a typical pattern in HUVECs, under either basal or stimulated conditions: the alpha form was predominant over the beta form and the cell-associated IL-1s measured were more abundant than the material recovered in the supernatants. Bacterial lipopolysaccharide (LPS, 0.5-5 micrograms/ml) significantly increased the basal production of IL-1. Pulses of recombinant IL-1 alpha or -beta or of TNF-alpha followed by a 24 h culture period were also associated with an increased endothelial production of IL-1, with a higher proportion of material secreted in the supernatants as compared with LPS. Other cytokines applied as pulses failed to induce the IL-1s or to modify LPS-induced production of IL-1: they include IL-2, immune interferon, GM-CSF, TGF-beta and EGF. Pharmacological modulators of LPS-induced IL-1 production were identified: glucocorticoids were inhibitors whereas retinoic acid and 1.25-dihydroxy-vitamin D3 had no effects and prostaglandin E2 and IBMX were weak inhibitors. There is no evidence that IL-1 alpha and IL-1 beta are regulated differently in HUVECs, but several significant differences from the monocyte were observed in the regulation of HUVEC IL-1 production.
1-Methyl-3-isobutylxanthine↗
Desensitization to vasopressin action in the rat kidney medulla: studies on isolated nephron segments.
Because of the prominent role of the renal medulla in the elaboration of concentrated urine and the possible differential regulation of the various nephron segments, desensitization to vasopressin (AVP) was studied on freshly isolated rat medullary thick ascending limbs (MTALs) and outer medullary collecting ducts (MCDs). Desensitization was induced through intramuscular injections of 1-deamino-8-D-arginine-vasopressin (dDAVP, 2 micrograms/day for 3 days), the last of which was performed 1 h before kidney removal. The cellular response to AVP was studied by measuring cAMP accumulation in micro-dissected nephron segments. In the MTAL, we observed a marked (around 80%) and selective desensitization to AVP, the response to either glucagon or human calcitonin remaining unaltered. In the MCD, significant desensitization was observed in the presence of 1 nM AVP in the assay medium, and was no longer significant when the AVP concentration was increased to supramaximal levels (10-1,000 nM). These experiments thus reveal a clear dissociation between MTAL and MCD with regards to dDAVP-induced desensitization and extend previous observations made on target segments in the renal cortex.
Animals↗
Arachidonate metabolism triggered in primed macrophages by signals inducing antitumor activity.
The acquisition of antitumoral functions by mouse peritoneal macrophages is controlled by the addition of activating agents (lipopolysaccharide (LPS), muramyldipeptide (MDP) or A23187), on appropriately primed macrophages. The release of eicosanoids during this activation step was examined by radio-HPLC. We demonstrated that the induction of antitumor activity in primed macrophages by LPS or MDP was associated with the release of 20:4 derivatives; arachidonic acid was metabolized predominantly via the cyclooxygenase pathway to PGE2 and thromboxane. The production of PGE2, quantified by an enzyme immunoassay, was sustained and important (up to 20 ng/ml/h/10(6) macrophages). However, PGE2 and thromboxane did not seem essential to the activation process: induction of antitumor activity took place and was even enhanced in the presence of indomethacin, whereas it was decreased by exogenous PGE2. During culture in vitro, primed macrophages released spontaneously significant amounts of 20:4 metabolites and became unresponsive to activation stimuli. Again indomethacin had a positive effect: it protected primed macrophages against this loss of activability. Cyclooxygenase metabolites released in response to activating stimuli or spontaneously seem to trigger deactivation pathways.
Acetylmuramyl-Alanyl-Isoglutamine↗