Microsoft Word - NEF334BF.rtf

Noriaki Yorioka, MD, 2nd Department of Internal Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima City 734 (Japan) Dear Sir, Based on the hypothesis of Moorhead et al. [1], abnormalities of the lipid metabolism are now considered aggravating factors for glomerulonephritis. Low-density lipoprotein (LDL), a cholesterol-rich lipoprotein, attracted attention, initially, and many reports appeared on LDL as a proliferation factor in cultured mesangial cells [2-4]. The presence of LDL receptors and scavenger receptors in mesangial cells has been proved [3, 4], and the uptake of LDL by mesangial cells has been confirmed using an isotopebinding method and the fluorescent antibody technique [3, 5, 6]. It is also known that mesangial cells, with incorporated LDL, secrete various chemical mediators and alter the mesangial microen-vironment [7]. For example, there are reports on the expression of messenger RNA of growth factors and cytokines such as platelet-derived growth factor [2] and macro-phage chemoattractant protein 1 [8], extracellular matrix such as fibronectin [8] and type IV collagen [9], and eicosanoids such as PG-E2 [4] from mesangial cells when stimulated with LDL or oxidized LDL. A cyto-toxic effect of oxidized LDL on mesangial cells and the mechanism of progression to glomerulosclerosis due to this cytotoxicity have been proposed [7, 10]. However, no reports have appeared, as yet, on the action of the triglyceride-rich intermediate-density lipoprotein (IDL) on the mesangial cells. Therefore, we observed the effects on DNA synthesis in mesangial cells stimulated by IDL. The method involved isolation and culture of human mesangial cells as previously 1,400 g 1,200 o 1,000 600 400 200 5 10 50 100 500 1,000 IDL (μg/ml)