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Although oxidative stress has been long associated with the genesis and progression of the atherosclerotic plaque, scanty data on its in situ effects on protein sulfhydryl group modifications are available. Within the arterial wall, protein sulfhydryls and low-molecular-weight (LMW) thiols are involved in the cell regulation of both Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) levels and are a target for several posttranslational oxidative modifications that take place inside the atherosclerotic plaque, probably contributing to both atherogenesis and atherosclerotic plaque progression towards complicated lesions. Advanced carotid plaques are characterized by very high intraplaque GSH levels, due to cell lysis during apoptotic and/or necrotic events, probably responsible for the altered equilibrium among protein sulfhydryls and LMW thiols. Some lines of evidence show that the prooxidant environment present in atherosclerotic tissue could modify filtered proteins also by protein-SH group oxidation, and demonstrate that particularly albumin, once filtered, represents a harmful source of homocysteine and cysteinylglycine inside the plaque. The oxidative modification of protein sulfhydryls, with particular emphasis to protein thiolation by LMW thiols and its association with atherosclerosis, is the main topic of this review.

Cardiovascular diseases are the leading cause of mortality and morbidity in developed countries being atherosclerosis the major contributor. Atherosclerosis is a form of chronic inflammation characterized by the accumulation of lipids and fibrous elements in medium and large arteries (Libby, 2002). The retention of apoB-100 containing lipoproteins (mainly LDL and Lp(a)) in the subendothelial space and their subsequent oxidation is thought to be the leading event in the development of atherosclerotic lesions (Williams & Tabas, 1995). The degree of inflammation, proteolysis, calcification and neovascularization affects the stability of advanced lesions. Plaque rupture and thrombosis are the most important clinical complications in the pathogenesis of stroke, coronary arteries and peripheral vascular diseases (Lutgens et al., 2003). So, the identification of early biomarkers of plaque presence and susceptibility to ulceration could be of primary importance in preventing such a lifethreatening event. Disease aetiology is very complex and includes several important environmental and genetic risk factors such as hyperlipidemia, diabetes, and hypertension. In this regard elevated plasma levels of LDL cholesterol and low levels of HDL cholesterol have been long associated with the onset and development of atherosclerotic lesions. Although enormous efforts have been done to elucidate the molecular mechanisms underlying plaque formation and progression, they are not yet completely understood. In the last years, proteomic studies have been undertaken to both elucidate pathways of atherosclerotic degeneration and individuate new circulating markers to be utilized either as early diagnostic traits or as targets for new drug therapies. This chapter will provide an overview of latest advances in proteomic studies on atherosclerosis and some related diseases, with particular emphasis on vascular tissue proteomics and lipoproteomics.

Aim of this paper is to report on a screening on sponge ECM glycosaminoglycan (GAG) diversity. To investigate the heterogeneity of sponge extracellular sulphated glycans, we determined their content and distribution in some Mediterranean and Caribbean species. To focus on biological and morpho-functional roles of these molecules in the sponge ECM some selected species were considered as models to investigate the topographic distribution of GAGs in sponge body according with the different architecture of specialized regions.

Diabetes and atherosclerosis are two chronic pathologies which prevalence is constantly growing worldwide, leading to disability and life-threatening complications. Since their consequences represent major causes of mortality and morbidity in developed countries, the identification and characterisation of new potential biomarkers may contribute to revealing the underlying mechanisms of pathology onset and progression, and to improving the diagnostic methodologies and the therapeutic approaches used for the treatment of these pathological conditions. A method recently developed was applied to urine from type 1 and type 2 diabetes patients and healthy controls for quantitation and structural characterisation of Urinary Trypsin Inhibitor (UTI), evidencing higher levels of this proteoglycan in both classes of patients with respect to controls. Furthermore, mass spectrometry (MS) analysis revealed oxidative post-translational modifications, which may affect UTI localization, function and pathophysiological activity. Lipoproteomics of purified plasma VLDL, LDL and HDL fractions from both patients undergoing carotid endarterectomy and healthy controls was performed by 2-DE coupled with MS, allowing the identification of Acute Phase-SAA as a potential biomarker of advanced atherosclerotic lesions. A role of LDL as Acute Phase-SAA carrier into the subendothelial space of arteries was also suggested.