Ah&actConditioned media of human glial cell lines induced alkaline phosphatase activity in cultured calf artery endothelial cells. The maximal alkaline phosphatase activity in the culture was comparable to the level in isolated brain capillary endothelial cells. An induction factor in the conditioned media was purified and identified as interleukind from its amino-terminal sequence, molecular weight, amino acid composition and immunoreactivity. Recombinant interleukin-6 had similar induction activity. Our findings raise the possibility that interleukin-6 induces and modulates alkaline phosphatase activity in endothelial cells during normal development of the blood-brain barrier and under certain pathological conditions.

An enzyme-linked immunosorbent assay, based on two monoclonal antibodies (Hreg1-1 and Hreg101-1) specific for pancreatic stone protein (PSP)/reg-protein, was developed to determine the concentration of this protein in serum from individuals with various diseases. The serum concentration of PSP/reg-protein was significantly higher in patients with various pancreatic diseases than in normal controls, and was also significantly higher in patients with acute pancreatitis or chronic relapsing pancreatitis than in patients with chronic pancreatitis. Furthermore, the serum PSP/reg-protein concentration was also significantly increased in liver cirrhosis, choledocholithiasis, and various cancers of the digestive system, and was extremely high in all patients tested with chronic renal failure. A significant correlation was apparent between the serum concentration of PSP/reg-protein and elastase-I in 68 patients with chronic pancreatitis or pancreatic cancer. Whereas only 7 of these patients showed a normal serum PSP/reg-protein concentration and a significantly increased elastase-I concentration, 15 of these patients showed a significantly increased serum PSP/reg-protein concentration and a normal serum elastase-I concentration. These results indicate that the serum PSP/reg-protein concentration may reflect pancreatic damage, especially in acute pancreatitis, and may be a sensitive a marker for such damage as elastase-1, although false positivity was apparent in renal failure and in some patients with hepatic dysfunction or digestive system malignancies.

No abstract

We prepared a monoclonal antibody (MAb 1-168) which recognizes the endothelial cells in the rabbit atherosclerotic aorta, by immunizing mice with the homogenate of atherosclerotic aorta of rabbits fed a high cholesterol diet. Indirect immunofiuorescence microscopy of the cryosections revealed that MAb 1-168 exclusively stained the endothelial cells overlying the lesions. Specific immunofluorescences were observed in the cytoplasm as dot or stripe-like patterns. In contrast, specific immunolabellings were scarcely detected in the endothelial cells overlying the nonlesional area in the aorta of cholesterol-fed and normal rabbits. MAb 1-168 also stained cultured porcine endothelial cells. Relatively weak fluorescences were observed along the cell periphery and stress fibers. The molecular weight of the antigenic material was identified as 40 kDa by SDS-PAGE and Western blot analysis of cultured porcine endothelial cells and rabbit atherosclerotic lesions. These findings suggest that the antigenic material may be an actin cytoskeleton-related substance that increased in the endothelial cells overlying the atherosclerotic plaques.A During the pathogenesis of atherosclerosis, the intima of arteries becomes thickened because of foam cell accumulation and smooth muscle cell proliferation. Damage or dysfunction of the arterial endothelial layer is also considered to be one of the most important events in the development of atherosclerotic lesions (17, 18). Using animal models, many investigators have demonstrated atherogenesis-related endothelial functional alterations such as the adhesion of blood cells to the endothelium