PubMed · 6417733
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G R de Lima, E Baracat. [Hormonal contraception].. https://pubmed.ncbi.nlm.nih.gov/6417733/
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The neutrophil agonist neutrophil-activating peptide-2 (NAP-2) arises through proteolytic processing of platelet-derived N-terminally extended inactive precursors, the most abundant one being connective tissue-activating peptide-III (CTAP-III). Apart from N-terminal processing, C-terminal processing also appears to participate in the functional regulation of NAP-2, as indicated by our recent identification of an isoform missing four C-terminal amino acids, NAP-2 (1-66), which was about threefold more potent than full-size NAP-2. In the present study, we report on the discovery and identification of natural NAP-2 (1-63), an isoform truncated by seven C-terminal residues. Functional and receptor-binding analyses demonstrated that NAP-2 (1-63) represents the most active isoform, being about fivefold more potent than full-size NAP-2. Analyses of rNAP-2 isoforms successively truncated at the C terminus by up to eight residues suggest functionally important roles for acidic residues and for the leucine at position 63, a residue highly conserved within CXC chemokines. Finally, we report on a novel C-terminally truncated isoform of CTAP-III (CTAP-III (1-81)) representing the potential precursor of NAP-2 (1-66). We show that C-terminal truncation in CTAP-III enhances its potency to desensitize chemokine-induced neutrophil activation, indicating that C-terminal processing might not only serve to enhance neutrophil activation, but might as well participate in the down-regulation of an inflammatory response.
NEW CARDIOVASCULAR RISK FACTORS: A causal link would appear to exist between hemostasis and cardiovascular disease. This is particularly true for fibrinogen which is an independent risk factor. MULTIPLE INTERACTIONS: There is an association between elevated triglyceride and FVIIc (pro-coagulant) levels and hypofibrinolytic PAI-1. In addition, an association exists between elevated cholesterol and FVIIc and platelet activation. LIPID LOWERING DRUGS AFFECT HEMOSTASIS: The hemostasis equilibrium is modulated by diet. In addition, fibrinogen levels are lowered by fibrates and platelet activation and thrombin generation are decreased by statins. These modifications have a potential clinical interest. Such observations remain to be confirmed by cardiovascular prevention studies with the specific objective of evaluating the effect of lipid lowering drugs on hemostasis parameters.