Analysis of Soluble Molecular Fibronectin-Fibrin Complexes and EDA-Fibronectin Concentration in Plasma of Patients with Atherosclerosis

Abstract

Atherosclerosis, a chronic vascular disease, leads to molecular events bound with interplaying processes of inflammation and coagulation. In the present study, fibronectin (FN), FN containing extra domain A (EDA-FN), frequency of occurrence, and relative amounts of soluble plasma FN-fibrin complexes were analyzed in 80 plasma samples of patients suspected of coronary artery disease based on clinical evaluation and changes in arteries found by computed tomographic coronary angiography. The study showed that in the plasma of the patients’ group with high risk of coronary artery disease EDA-FN concentration was significantly higher (3.5 ± 2.5 mg/L; P < 0.025) and the molecular FN-fibrin complexes of 1000 kDa and higher occurred more often than in the groups of patients with mild risk of coronary artery disease and the normal age-matched. The increased level of EDA-FN and occurrence of FN-fibrin complexes could have a potential diagnostic value in the diagnosis and management of patients with coronary artery disease.

The extra domain A of fibronectin facilitates osteoclastogenesis in radicular cysts through vascular endothelial growth factor

“…This could be attributed to myofibroblast differentiation, in which EDA + FN plays an essential role (White et al ). Myofibroblasts always appear in the fibrous capsule of various odontogenic cysts (Kouhsoltani et al ) as the result of chronic inflammation or inappropriate wound healing (Lemanska‐Perek et al ). Fibroblasts of odontogenic cysts have been demonstrated as favourable for osteoclast formation in previous studies (Wang & Li , Wang et al 2015a, Wang et al 2015b).…”

“…According to previous studies, fibroblasts isolated from the fibrous capsule of odontogenic cysts induce more osteoclasts than do normal controls (Wang & Li 2013, Wang et al 2015a, possibly attributed to the differentiation of myofibroblasts, which are activated during chronic inflammation (Kouhsoltani et al 2016) or inappropriate wound healing (Lemanska-Perek et al 2016). Chronic inflammation may initiate radicular cysts that can also activate fibroblasts in capsules, generating extracellular matrix (ECM; Jiang et al 2014), cellular factors and metabolic products (de Moraes et al 2011, Tekkesin et al 2011, Bernardi et al 2015, leading to osteoclastogenesis and bone destruction, as illustrated by radiolucent periapical areas.…”

Time‐dependent changes in extra‐domain A‐fibronectin concentration and relative amounts of fibronectin‐fibrin complexes in plasma of patients with peripheral arterial disease after endovascular revascularisation

“…15 EDA-FN with its known proinflammatory and pro-thrombotic activities 15 is secreted at high concentrations into the plasma of PAD patients during the first and second stages after revascularisation (Table 1) and with disease progression and restenosis occurrence ( Figure 4B). Some changes in EDA-FN concentration have also been found in the plasma of patients with advanced coronary artery disease, 27 thrombosis, 15,38 and diabetes. [39][40][41] Diabetes and ulceration were reported to be associated with increased deposition of FN in ECM and linked with the occurrence of FN modified by glycation and/or hypoxia.…”

“…FN‐fibrin complexes were also found in human blood plasma and were demonstrated by agarose immunoblotting under semi‐denaturing, non‐reducing conditions as a series of FN‐fibrin bands with molecular masses from 750 to 2100 kDa . Such macromolecular complexes were demonstrated by Kątnik‐Prastowska's group in the plasma of patients with recurrent respiratory infections, atherosclerosis with advanced coronary artery disease, aging, and also multi‐morbidity, especially when coexisting with cardiovascular diseases and osteoarthrosis but rarely in healthy individuals . It is postulated that their occurrence might be related to molecular events connected with interplaying processes of inflammation, immunity, and coagulation and/or may also be involved in fibrin clearance from the circulation in inflammatory conditions …”

“…25 Such macromolecular complexes were demonstrated by Kątnik-Prastowska's group in the plasma of patients with recurrent respiratory infections, 25 atherosclerosis with advanced coronary artery disease, 26 aging, and also multi-morbidity, especially when coexisting with cardiovascular diseases and osteoarthrosis 16 but rarely in healthy individuals. 15,[25][26][27] It is postulated that their occurrence might be related to molecular events connected with interplaying processes of inflammation, immunity, and coagulation 27 and/or may also be involved in fibrin clearance from the circulation in inflammatory conditions. 28 Witkiewicz and coworkers have analysed some inflammatory and haemostatic parameters in the plasma of patients with advanced PAD of the lower extremities after endovascular revascularisation and in relation to new restenosis.…”