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

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 14 C-glycosaminoglycan ( 14 C-GAG) and 3 H-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.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/37798/1/1780360816_ftp.pd