This is further supported by the finding that the 38 kDa PRELP protein was not detected in serum and thus probably not secreted by CLL cells. Rapid degradation of the 38 kDa PRELP in serum by proteases could however not be excluded. Recombinant PRELP expressed in SP2/0 cells, was detected by our polyclonal C-terminal antibody as weak bands of 38, 44, 48 kDa and a major band of 55-58 kDa. This is assumed to represent varying degrees of glycosylation. Our anti-PRELP mAbs, recognized however only the 38 kDa band. An explanation might be that our mAbs recognized epitopes that are hidden in the mature PRELP three-dimensional folding. This is the first report connecting PRELP with CLL. There are reports linking other SLRPs to cancer. We have previously reported on the unique CLL expression of the closely related SLRP FMOD. SLRPs are normally secreted proteins that mediate their functions by binding to membrane receptors or extracellular matrix proteins. However, other locations and functions have been reported. PRELP has been shown to bind and inhibit NF-kappa B activity in the nucleus of osteoclasts. Our findings suggest the presence of a predominant, nonsecreted unglycosylated 38 kDa variant of PRELP in CLL cells. The specific expression of another structurally related proteoglycan, FMOD, in CLL as well as a third SLRP. Functional characterization of proteoglycans in CLL is warranted to understand their biological importance in the pathogenesis of CLL. Atherosclerosis is a chronic multifactoral inflammatory disease involving elastic and muscular arteries. The inflammatory response of the vascular wall is thought to involve uncontrolled proliferation of vascular myointimal cells, production of foam cells, and progressive vascular occlusion. The inflammatory cells in atherosclerotic lesions produce various cytokines including IL-1b, TNF-a, IL-6, MCP-1 so on, and these complex cytokine networks contribute to formation of atherosclerotic lesion. The atherosclerotic processes in human continue for long time with high complexity. Furthermore, it is almost impossible to perform direct analysis of the atherosclerotic lesion from an individual patient. Therefore, several animal AbMole 4-(Benzyloxy)phenol models including mouse, rat, rabbit, and pig have been used to understand the complicated processes of atherosclerosis. Especially, mouse models have been widely used for understanding of atherosclerosis, and instrumental in evaluating new atherosclerotic drugs. Since wild type mice are highly resistant to atherosclerosis due to the high levels of antiatherosclerotic HDL, several transgenic and knockout mouse models were developed to increase the susceptibility to atherosclerosis. The most widely used mouse models for atherosclerosis are apolipoprotein E-deficient and LDL receptor-deficient mice, and have contributed to understand the mechanisms of atherogenesis.