Connective tissue activation. xxxvi. the origin, variety, distribution, and biologic fate of connective tissue activating peptide–iii isoforms: characteristics in patients with rheumatic, renal, and arterial disease

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Abstract
Objective. To determine the origin, distribution, and biologic fate of platelet‐derived connective tissue activating peptide–III (CTAP‐III), to define the relative amounts of the antigen forms (CTAP‐III, betathromboglobulin [β‐TG], neutrophil activating peptide–2 [NAP‐2]) in plasma of normal persons and those with rheumatic or end‐stage renal disease, and to define the isoforms of CTAP‐III in platelets, plasma, transudates, and tissue deposits.Methods. CTAP‐III in plasma was measured by enzyme‐linked immunosorbent assay, and growth promoting activity of CTAP‐III isoforms was tested in synovial and peritoneal cell cultures by measuring increased synthesis of 14C‐glycosaminoglycan (14C‐GAG) and 3H‐DNA. Isolated CTAP‐III was characterized by Western blotting, microsequencing, and mass spectrometry.Results. CTAP‐III was the primary isoform of this antigen family in normal platelets and platelet‐rich plasma; β‐TG and NAP‐2 accounted for 90%), and β‐TG was the most rare (0–1%). Deposition of CTAP‐III in tissues, such as synovium, spleen, and kidney, is associated with partial processing to NAP‐2–like isoforms and the potential to induce neutrophil and fibroblast activation in patients with rheumatic or end‐stage renal disease.