Fibronectin is Synthesized as an Acute Phase Reactant in Rat Hepatocytes

Abstract

Summary: Elevated concentrations of fibronectin were found in plasma of rats under different acute phase conditions. Untreated animals showed a plasma fibronectin concentration of 150 + 50 mg/1, which increased to 412 ± 59 mg/1 24 h after subcutaneous injection of turpentine. The time course of the changes in plasma fibronectin concentration showed a peak at 24 h and a decline to norinal concentrations 72 h after turpentine treatment. Additional Stimulation by dexamethasone resulted in plasma fibronectin concentrations of 661 ± 49 mg/1. No or only slight elevations of fibronectin concentrations were observed after treatment with adrenaline, thyroxine and triiodothyronine äs compared with saline-injected animals. The common identity of plasma fibronectin in Controls, turpentine and turpentine-dexamethasone-treated animals was shown by slab gel electrophoresis under nonreducing conditions, followed by western blot and immunofluorescence staining. One dimensional immunoelectrophoresis performed with polyclonal antibodies to human fibronectin cross-reacting with rat fibronectin (shown by Ouchterlony gel diffusion) revealed indentical precipitation lines for the plasma of control and acute phase animals. Hepatocytes of turpentine-pretreated rats show a threefold increase of [ 14 C]valine incoiporation into total protein and a fourfold increase of immunoreactive radioactively labeled fibronectin in the culture medium, compared with control hepatocyte cultures. These results point to the role of hepatocytes in the synthesis of plasma fibronectin, which behaves in rats äs an acute phase reactant.

Glomerular compromise in mercuric chloride-induced nephrotoxicity

“…The sections were then incubated with a polyclonal rabbit antibody to human fibronectin (kindly supplied by Dr. Agueda Rostagno, Department of Pathology, New York University Medical Center, New York) (dilution 1:200 in PBS containing BSA and triton X-100), 30 minutes. Cross-reactivity between rat fibronectin and antibody to human fibronectin, previously reported by Pick-Kober et al (16), and specificity were determined by Ouchterlony, immunoelectrophoresis, and enzyme-linked immunosorbent assay (ELISA) against affinity chromatography purified human fibronectin and human and rat plasma. For the visualization of the antibody reaction, a second antibody antirabbit Ig conjugated with peroxidase was added to the sections.…”

Rabbit Plasma Fibronectin Levels Associated withStaphylococcusaureusEnterotoxin B: An Acute-Phase Reaction

“…Fn appears to be important in the early phase of inflammation, because increased levels are part of an acute-phase reaction [11], It is not clear why rabbits given cryoprecipitate prophylaxis had plasma Fn levels and WBC counts no different from the unsupplemented treatment group. It is possible that the amount of cryo precipitate injected was not sufficient to offer an advan tage.…”

“…Fibronectin (Fn), a high-molecular-weight glycopro tein, is a major component of blood, body fluids and connective tissue and has been reported to interact with fibrin, heparin, collagen, Fibrinogen, actin and some bac teria [1], It mediates the attachment of Staphylococcus aureus to human neutrophils [2], Fn levels decrease in sepsis and trauma [3,4], and this may be related to wound healing, because it aids in cleaning up cellular debris and binds toxins to macrophages [5][6][7][8], Plasma Fn levels increased 100% following casein-induced ex perimental peritonitis in rats, and intraperitoneal inocu lation with 1010 S. aureus cells also causes an initial ele vation in plasma Fn levels, suggesting that increased Fn levels represent an acute-phase reaction [9][10][11].…”

Correlations between plasma levels of a fibronectin isoform subpopulation and C-reactive protein in patients with systemic inflammatory disease

“…Specifically, the majority of TFN is an acute phase reactant derived from the liver (Tamkun et al 1983, Amrani et al 1986, Pick-Kober et al 1986, Hynes 1990), whereas A + FN is normally concentrated in blood vessel walls (Vartio et al 1987, Peters et al 1996). Therefore, potential sources of soluble circulating A + FN in health and disease include vascular endothelial cells, which have been observed to express EIIIA segment-enriched FN in vitro (Peters et al 1990), and platelets, in which A + FN is similarly enriched relative to the total pool of alpha granule FN (Paul et al 1986, Peters et al 1995).…”