Identification and distribution of fibrinogen, fibrin, and fibrin(ogen) degradation products in atherosclerosis. Use of monoclonal antibodies.

TLDR

The study used ABC‑immunoperoxidase staining with monoclonal antibodies 18C6, T2G1, and GC4 to map fibrinogen/fibrin I, fibrin II, and fibrin(ogen) degradation products in normal and atherosclerotic vessels. Normal aortas showed negligible fibrinogen/fibrin I or II and no degradation products, whereas early lesions and fibrous plaques contained fibrinogen/fibrin I and II in threads and around cells, and fibrous/advanced plaques displayed all three forms—including degradation products—in loose connective tissue, thrombus, and near cholesterol crystals, indicating that increased fibrin formation and degradation accompanies atherosclerotic progression and may involve local cellular conversion of fibrinogen to fibrin.

Abstract

Samples of normal and atherosclerotic vessels obtained from vascular and cardiothoracic surgery were examined for the distribution of fibrinogen/fibrin I, fibrin II, and fibrin(ogen) degradation products (Fragment D/DD) by using recently characterized monoclonal antibodies that recognize and distinguish the three molecular forms (MAbs 18C6, T2G1, and GC4, respectively) with the ABC-immunoperoxidase technique. In normal aortas, little fibrinogen/fibrin I or fibrin II was present and no fibrin(ogen) degradation products could be detected. In early lesions and in fibrous plaques, fibrinogen/fibrin I and fibrin II were distributed in long threads and surrounding vessel wall cells and macrophages. Fibrin(ogen) degradation products were not seen in early lesions. In fibrous and advanced plaques, fibrinogen/fibrin I, fibrin II, and fibrin(ogen) degradation products were detected in areas of loose connective tissue, in thrombus, and around cholesterol crystals. The results of this study suggest that increased fibrin formation and degradation may be associated with progression of atherosclerotic disease. The observed distribution of the different molecular forms of fibrinogen also suggests the possibility that the cells present in the lesions actively participate in the fibrinogen-to-fibrin transition within the vessel wall.